Duffy antigen system

Duffy antigen system
Duffy blood group, chemokine receptor
Symbols DARC; CCBP1; CD234; Dfy; FY; GPD
External IDs OMIM613665 MGI1097689 HomoloGene48067 IUPHAR: FY GeneCards: DARC Gene
Species Human Mouse
Entrez 2532 13349
Ensembl ENSG00000213088 ENSMUSG00000037872
UniProt Q16570 QLOVE
RefSeq (mRNA) NM_002036 NM_010045
RefSeq (protein) NP_002027 NP_034175
Location (UCSC) Chr 1:
159.17 – 159.18 Mb
Chr 1:
175.17 – 175.17 Mb
PubMed search [1] [2]

Duffy antigen/chemokine receptor (DARC) also known as Fy glycoprotein (FY) or CD234 (Cluster of Differentiation 234) is a protein that in humans is encoded by the DARC gene.[1][2][3]

The Duffy antigen is located on the surface of red blood cells and is named after the patient in which it was discovered. The protein encoded by this gene is a glycosylated membrane protein and a non-specific receptor for several chemokines. The protein is also the receptor for the human malarial parasites Plasmodium vivax and Plasmodium knowlesi. Polymorphisms in this gene are the basis of the Duffy blood group system.[4]



It was noted in the 1920s that black Africans had some intrinsic resistance to infection with malaria but the basis for this remained unknown. The Duffy antigen gene was the fourth gene associated with the resistance after the genes responsible for sickle cell anaemia, thalassemia and glucose-6-phosphate dehydrogenase.

In 1950 the Duffy antigen was discovered in a multiply transfused hemophiliac whose serum contained the first example of anti-Fya antibody.[5] In 1951 the antibody to a second antigen, Fyb, was discovered in serum. Using these two antibodies three common phenotypes were defined: Fy(a+b+), Fy(a+b-), and Fy(a-b+).

Several other types were later discovered bringing the current total up to 6: Fya, Fyb, Fy3, Fy4, Fy5 and Fy6. Only Fya, Fyb and Fy3 are considered clinically important. Reactions to Fy5 have also rarely been reported.

Genetics and genomics

The Duffy antigen /chemokine receptor gene (gp-Fy; CD234) is located on the long arm of chromosome 1 (1.q22-1.q23) and was cloned in 1993.[2] The gene was first localised to chromosome 1 in 1968 and was the first blood system antigen to be localised. It is a single copy gene spanning over 1500 bases and is in two exons. It encodes a 336 amino acid acidic glycoprotein. The gene carries the antigenic determinants of the Duffy blood group system which consist of four codominant alleles—FY*A and FY*B—coding for the Fy-a and Fy-b antigens respectively, FY*X and FY*Fy, five phenotypes (Fy-a, Fy-b, Fy-o, Fy-x and Fy-y) and five antigens. Fy-x is a form of Fy-b where the Fy-b gene is poorly expressed. Fy-x is also known as Fy-bweak or Fy-bWk.

Fy-a and Fy-b differ by in a single amino acid at position 42: glycine in Fy-a and aspartic acid in Fy-b (guanine in Fy-a and adenosine in Fy-b at position 125). A second mutation causing a Duffy negative phenotype is known: the responsible mutation is G -> A at position 298. The genetic basis for the Fy(a-b-) phenotype is a point mutation in the erythroid specific promoter (a T -> C mutation at position -33 in the GATA box). This mutation occurs in the Fy-b allelle and has been designated Fy-bEs (erythroid silent). Two isotypes have been identified. The Fy-x allelle is characterized by a weak anti-Fy-b reaction and appears to be the result of two separate transitions: Cytosine265Threonine (Arginine89Cysteine) and Guanine298Adenosine (Alanine100Threonine). A third mutation (a transversion) in this gene has also been described - G145T (Alanine49Serine) - that has been associated with the Fy-x phenotype.

Most Duffy negative blacks carry a silent Fy-b allele with a single T to C substitution at nucleotide -46, impairing the promoter activity in erythroid cells by disrupting a binding site for the GATA1 erythroid transcription factor. The gene is still transcribed in non erythroid cells in the presence of this mutation.

The Duffy negative phenotype occurs at low frequency among whites (~3.5%) and is due to a third mutation that results in an unstable protein (Arg89Cys: cytosine -> thymidine at position 265).[6]

The silent allele has evolved at least twice in the black population of Africa and evidence for selection for this allele has been found.[7] The selection pressure involved here appears to be more complex than many text books might suggest.[8] An independent evolution of this phenotype occurred in Papua New Guinea has also been documented.[9]

A comparative study of this gene in seven mammalian species revealed significant differences between species.[10] The species examined included Pan troglodytes (chimpanzee), Macaca mulatta (rhesus monkey), Pongo pygmaeus (orangutan), Rattus norvegicus (brown rat), Mus musculus (mouse), Monodelphis domestica (opposum), Bos taurus (cow) and Canis familiaris (dog).

Three exons are present in humans and chimpanzees while only two exons occur in the other species. This additional exon is located at the 5' end and is entirely non coding. Both intron and exon size varies considerably between the species examined. Between the chimpanzee and the human 24 differences in the nucleotide sequence were noted. Of these 18 occurred in non coding regions. Of the remaining 6, 3 were synonymous and 3 non synonymous mutations. The significance of these mutations if any is not known.

The mouse ortholog has been cloned and exhibits 63% homology to the human gene at the amino acid level. The mouse gene is located on chromosome 1 between the genetic markers Xmv41 and D1Mit166. The mouse gene has two exons (100 and 1064 nucleotides in length respectively), separated by a 461 base pair intron. In the mouse DARC is expressed during embryonic development between days 9.5 and 12.

In yellow baboons (Papio cynocephalus) mutations in this gene have been associated with protection from infection with species of the genus Hepatocystis.[11]

Molecular biology

The Duffy antigen is expressed in greater quantities on reticulocytes than on mature erythrocytes.[12] While the Duffy antigen is expressed on erythrocytes it is also found on some epithelial cells, Purkinje cells of the cerebellum,[13] endothelial cells of thyroid capillaries, the post-capillary venules of some organs including the spleen, liver and kidney[14] and the large pulmonary venules. In some people who lack the Duffy antigen on their erythrocytes it may still be expressed in some cells.[15] It has two potential N-linked glycosylation sites at asparagine (Asn) 16 and Asn27.

The Duffy antigen has been found to act as a multispecific receptor for chemokines of both the C-C and C-X-C families, including:

  • monocyte chemotatic protein-1 (MCP-1) - CCL2[16]
  • regulated upon activation normal T expressed and secreted (RANTES) - CCL5[17]
  • melanoma growth stimulatory activity (MSGA-α), KC, neutrophil-activating protein 3 (NAP-3) - CXCL1/CXCL2[18]

and the angiogenic CXC chemokines:

  • growth related gene alpha (GRO-α) - CXCL1
  • ENA-78 - CXCL5
  • neutrophil activating peptide-2 (NAP-2) - CXCL7
  • interleukin-8 (IL-8) - CXCL8

Consequently the Fy protein is also known as DARC (Duffy Antigen Receptor for Chemokines). The chemokine binding site on the receptor appears to be localised to the amino terminus.[19] The antigen is predicted to have 7 transmembrane domains, an exocellular N-terminal domain and an endocellular C-terminal domain. Alignment with other seven transmembrane G-protein-coupled receptors shows that DARC lacks the highly conserved DRY motif in the second intracellular loop of the protein that is known to be associated with G-protein signaling. Consistent with this finding ligand binding by DARC does not induce G-protein coupled signal transduction nor a Ca2+ flux unlike other chemokine receptors. Based on these alignments the Duffy antigen is considered to be most similar to the interleukin-8B receptors.

Scatchard analysis of competition binding studies has shown high affinity binding to the Duffy antigen with dissociation constants (KD) binding values of 24 ± 4.9, 20 ± 4.7, 41.9 ± 12.8, and 33.9 ± 7 nanoMoles for MGSA, interleukin-8, RANTES and monocyte chemotactic peptide-1 respectively.[20]

In DARC-transfected cells, DARC is internalized following ligand binding and this led to the hypothesis that expression of DARC on the surface of erythrocytes, endothelial, neuronal cells and epithelial cells may act as a sponge and provide a mechanism by which inflammatory chemokines may be removed from circulation as well as their concentration modified in the local environment.[21] This hypothesis has also been questioned after knock out mice were created. These animals appeared healthy and had normal responses to infection. While the function of the Duffy antigen remains presently (2006) unknown, evidence is accumulating that suggests a role in neutrophil migration from the blood into the tissues[22] and in modulating the inflammatory response.[23][24][25][26][27][28][29][30][31][32]

The protein is also known to interact with the protein KAI1 (CD82) a surface glycoprotein of leukocytes and may have a role in the control of cancer.

The Duffy antigen has been shown to exist as a constitutive homo-oligomer and that it hetero-oligomerizes with the CC chemokine receptor CCR5 (CD195). The formation of this heterodimer impairs chemotaxis and calcium flux through CCR5, whereas internalization of CCR5 in response to ligand binding remains unchanged.[33]

DARC has been shown to internalise chemokines but does not scavenge them.[34] It mediates chemokine transcytosis, which leds to apical retention of intact chemokines and more leukocyte migration.

Binding melanoma growth-stimulating activity inhibits the binding of P. knowlesi to DARC.

Population genetics

Differences in the racial distribution of the Duffy antigens were discovered in 1954, when it was found that the overwhelming majority of blacks had the erythrocyte phenotype Fy(a-b-): 68% in African Americans and 88-100% in African blacks (including more than 90% of West African blacks).[35] This phenotype is exceedingly rare in whites. Because the Duffy antigen is uncommon in those of Black African descent, the presence of this antigen has been used to detect genetic admixture. In a sample of unrelated African Americans (n = 235), Afro-Caribbeans (n = 90) and Colombians (n = 93), the frequency of the -46T (Duffy positive) allele was 21.7%, 12.2% and 74.7% respectively.[36]

Overall the frequencies of Fya and Fyb antigens in Caucasians are 66% and 83% respectively, in Asians 99% and 18.5% respectively and in blacks 10% and 23% respectively. The frequency of Fy3 is 100% Caucasians, 99.9% Asians and 32% Blacks. Phenotype fequencies are:

Fy(a+b+): 49% Caucasians, 1% Blacks, 9% Chinese
Fy(a-b+): 34% Caucasians, 22% Blacks, <1% Chinese
Fy(a+b-): 17% Caucasians, 9% Blacks, 91% Chinese

While a possible role in the protection of humans from malaria had been previously suggested, this was only confirmed clinically in 1976.[37] Since then many surveys have been carried out to elucidate the prevalence of Duffy antigen alleles in different populations including:

  • The mutation Ala100Thr (G -> A in the first codon position—base number 298) within the FY*B allele was thought to be purely a Caucasian genotype, but has since been described in Brazilians. However, the study's authors point out that the Brazilian population has arisen from intermarriage between Portuguese, Black Africans, and Indians, which accounts for the presence of this mutation in a few members of Brazil's non-Caucasian groups. Two of the three Afro-Brazilian test subjects that were found to have the mutation (out of a total of 25 Afro-Brazilians tested) were also related to one another, as one was a mother and the other her daughter.[38]
  • This antigen along with other blood group antigens was used to identify the Basque people as a genetically separate group.[39] Its use in forensic science is under consideration.[40]
  • The Andaman and Nicobar Islands, now part of India, were originally inhabited by 14 aboriginal tribes. Several of these have gone extinct. One surviving tribe—the Jarawas—live in three jungle areas of South Andaman and one jungle area in Middle Andaman. The area is endemic for malaria. The causative species is Plasmodium falciparum: there is no evidence for the presence of Plasmodium vivax. Blood grouping revealed an absence of both Fy(a) and Fy(b) antigens in two areas and a low prevalence in two others.[41]
  • In the Yemenite Jews the frequency of the Fy allele is 0.5879[42] The frequency of this allelle varies from 0.1083 to 0.2191 among Jews from the Middle East, North Africa and Southern Europe. The incidence of Fya among Ashkenazi Jews is 0.44 and among the non-Ashkenazi Jews it is 0.33. The incidence of Fyb is higher in both groups with frequencies of 0.53 and 0.64 respectively.[43]
  • In the Chinese ethnic populations—the Han and the She people—the frequencies of Fya and Fyb alleles were 0.94 and 0.06 and 0.98 and 0.02 respectively.[44]
  • The frequency of the Fya allelle in most Asian populations is ~95%.
  • In Grande Comore (also known as Ngazidja) the frequency of the Fy(a- b-) phenotype is 0.86.[45]
  • In a survey of 115 unrelated Tunisians using both serological and DNA based methods gave the following results: FY*X frequency 0.0174; FY*1 = 0.291 (expressed 0.260, silent 0.031); FY*2 = 0.709 (expressed 0.427; silent 0.282). FY*2 silent is the most common allele in West African blacks and the high prevalence in this sample was interpreted as historical admixture.[46]
  • The incidence of Fy(a+b-) in northern India among blood donors is 43.85%.[47]
  • In Nouakchott, Mauritania overall 27% of the population are Duffy-positive. 54% of Moors are Duffy antigen positive, while only 2% of black ethnic groups (mainly Poular, Soninke and Wolof) are Duffy positive.[48]
  • A map of the Duffy antigen distribution has been produced.[49] The most prevalent allele globally is FY*A. Across sub-Saharan Africa the predominant allele is the silent FY*BES variant.

Clinical significance

Historically the role of this antigen other than its importance as a receptor for plasmodium parasitic protozoa has not been appreciated. Recent work has identified a number of additional roles for this protein.


Asthma is more common and tends to be more severe in those of African descent. There appears to be a correlation with both total IgE levels and asthma and mutations in the Duffy antigen.[50]

Benign ethnic neutropenia

A significant proportion (25–50%) of otherwise healthy African Americans are known to have a persistently lower white blood cell count than the normal range defined for individuals of European ancestry—a condition known as benign ethnic neutropenia. This condition is also found in Arab Jordanians, Black Bedouin, Falashah Jews, Yemenite Jews and West Indians. This condition is associated with a reduced capacity to mobilize bone marrow neutrophil reserves in response to corticosteroids, despite normal cellularity and maturation of all cell lines in bone marrow aspirates. Strongly suggestive evidence has been found that links condition to a mutation in the Duffy gene.[51] Although the mechanism is as yet unknown, it is known that neutrophils are retained in the bone marrow through interaction of CXCL12 with its receptor CXCR4. A number of rare diseases are known in which disruption or desensitization of CXCR4 results in failure to release mature neutrophils from bone marrow.


Interactions between the metastasis suppressor KAI1 on tumor cells and the cytokine receptor DARC on adjacent vascular cells suppresses tumor metastasis.[52] In human breast cancer samples low expression of the DARC protein is significantly associated with estrogen receptor status, both lymph node and distant metastasis and poor survival.[53]

Endotoxin response

The procoagulant response to lipopolysaccaride (bacterial endotoxin) is reduced in Duffy antigen negative Africans compared with Duffy positive Caucasians.[54] This erence is likely to involve additional genes.

HIV infection

A connection has been found between HIV susceptibility and the expression of the Duffy antigen. The absence of the DARC receptor appears to increase the susceptibility to infection by HIV. However once established, the absence of the DARC receptor appears to slow down the progression of the disease.[55]

HIV-1 appears to be able to attach to erythrocytes via DARC.[55]

The association between the Duffy antigen and HIV infection appears to be complex. Leukopenia (a low total white cell count) is associated with relatively poor survival in HIV infection and this association is more marked in caucasians than in negroids despite the (on average) lower white cell counts found in black Africans. This difference appears to correlate with a particular genotype (-46C/C) associated with the absence of the Duffy antigen.[56] This genotype has only been found in black Africans and their descendants. The strength of this association increases inversely with the total white cell count. The basis for this association is probably related to the role of the Duffy antigen in cytokine binding but this has yet to be verified.

A study of 142 black South African high-risk female sex workers over 2 years revealed a seroconversion rate of 19.0%.[57] Risk of seroconversion appeared to be correlated with Duffy-null-associated low neutrophil counts.

Lung transplantation

The Duffy antigen has been implicated in lung transplantation rejection.[58]


On erythrocytes the Duffy antigen acts as a receptor for invasion by the human malarial parasites P. vivax and P. knowlesi. This was first shown in 1980. Duffy negative individuals whose erythrocytes do not express the receptor are believed to be resistant to merozoite invasion[59] although it has been reported that P. vivax infection in Duffy negative children in Kenya, suggesting a role in resistance to disease, not infection.[59] This antigen may also play a role in erythrocyte invasion in the rodent malarial parasite P. yoelii. The epitope Fy6 is required for P. vivax invasion.[12]

The protection to P. vivax malaria conferred by the absence of the Duffy antigen appears to be very limited at best in Madagascar. Although 72% of the population are Duffy antigen negative, 8.8% of the Duffy antigen negative individuals were asymptomatic carriers of P. vivax.[60] Malaria has also been found in Angola and Equatorial Guinea in Duffy negative individuals.[61] P. vivax malaria in a Duffy antigen negative individual in Mauritania has also been reported.[62] Similar infections have been reported in Brazil[63][64] and Kenya.[59] Nancy Ma's night monkey (A. nancymaae) is used as an animal model of P. vivax infection. This species' erythrocytes possess the Duffy antigen and this antigen is used as the receptor for P. vivax on the erythrocytes in this species.[65]

Examination of this gene in 497 patients in the Amazonas State, Brazil, made by the doctor Sérgio Albuquerque, suggests that the genotypes FY*A/FY*B-33 and FY*B/FY*B-33 (where -33 refers to the null mutation at position -33 in the GATA box) may have an advantage over the genotypes FY*A/FY*B and FY*A/FY*A, FY*A/FY*B, FY*A/FY*X and FY*B/FY*X.[66] FY*A/FY*B and FY*A/FY*A genotypes showed to be associated with increased rates of P. vivax infection and FY*B/FY*X and FY*A/FY*X were shown to be associated with the low levels of parasitism.

Multiple myeloma

An increased incidence of Duffy antigen has been reported in patients with multiple myeloma compared with healthy controls.[67]


The Duffy antigen is present in the normal pulmonary vascular bed. Its expression is increased in the vascular beds and alveolar septa of the lung parenchyma during suppurative pneumonia.[22]


Duffy antigen has rarely been implicated in haemolytic disease of the newborn.

Prostate cancer

Experimental work has suggested that DARC expression inhibits prostate tumor growth. Men of black African descent are at greater risk of prostate cancer than are men of either Causcasian or Asian descendant (60% greater incidence and double the mortality compared to Caucasians). The reasons for this increased risk are not known. The contribution of DARC to this increased risk has been tested in Jamaican males of black African descent.[68] It was found that none of the increased risk could be attributed to the DARC gene.

Renal transplantion

Antibodies and a cellular response to the Duffy antigen have been associated with renal transplant rejection.[69]

Sickle cell anaemia

Duffy antigen negative individuals with sickle cell anaemia tend to suffer from more severe organ damage than do those with the Duffy antigen.[70] Duffy-positive patients exhibit higher counts of white blood cells, polynuclear neutrophils, higher plasma levels of IL-8 and RANTES than Duffy-negative patients.[71]

Southeast Asian ovalocytosis

There is a ~10% increase in Fy expression in Southeast Asian ovalocytosis erythocytes.[72]

Transfusion medicine

A Duffy negative blood recipient may have a transfusion reaction if the donor is Duffy positive.[36] Since most Duffy-negative people are of African descent, blood donations from people of black African origin are important to transfusion banks.

Transfusion data

International Society for Blood Transfusion (ISBT) symbol: FY

ISBT number: 008

Gene symbol: FY

Gene name: Duffy blood group

Number of Duffy antigens: 6

Antibody type: Almost entirely IgG. IgM does occur but is rare. These antibodies do not typically bind complement.

Transfusion reactions: Typically mild but may be serious. Although these usually occur immediately they may occur after a delay (up to 24 hours). These reactions are usually caused by Fya or Fyb. Fy3 may cause a reaction but only rarely.

Hemolytic disease of the newborn: This is typically mild but rarely may be serious. Almost always due to Fya: rarely Fyb or Fy3.


  1. ^ "Entrez Gene: DARC Duffy blood group, chemokine receptor". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=2532. 
  2. ^ a b Chaudhuri A, Polyakova J, Zbrzezna V, Williams K, Gulati S, Pogo AO (November 1993). "Cloning of glycoprotein D cDNA, which encodes the major subunit of the Duffy blood group system and the receptor for the Plasmodium vivax malaria parasite". Proc. Natl. Acad. Sci. U.S.A. 90 (22): 10793–7. Bibcode 1993PNAS...9010793C. doi:10.1073/pnas.90.22.10793. PMC 47864. PMID 8248172. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=47864. 
  3. ^ Tournamille C, Colin Y, Cartron JP, Le Van Kim C (June 1995). "Disruption of a GATA motif in the Duffy gene promoter abolishes erythroid gene expression in Duffy-negative individuals". Nat. Genet. 10 (2): 224–8. doi:10.1038/ng0695-224. PMID 7663520. 
  4. ^ "Entrez Gene: Duffy antigen". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=2532. 
  5. ^ Cutbush, Marie; Mollison, P.L.; Parkin, Dorothy M. (4 February 1950). "A New Human Blood Group" (PDF). Nature 165 (188–189): 188. Bibcode 1950Natur.165..188C. doi:10.1038/165188b0. http://www.nature.com/nature/journal/v165/n4188/pdf/165188b0.pdf. Retrieved 2007-06-08. 
  6. ^ Yazdanbakhsh K, Rios M, Storry JR, Kosower N, Parasol N, Chaudhuri A, Reid ME (March 2000). "Molecular mechanisms that lead to reduced expression of duffy antigens". Transfusion 40 (3): 310–20. doi:10.1046/j.1537-2995.2000.40030310.x. PMID 10738032. 
  7. ^ Hamblin MT, Di Rienzo A (May 2000). "Detection of the signature of natural selection in humans: evidence from the Duffy blood group locus". Am. J. Hum. Genet. 66 (5): 1669–79. doi:10.1086/302879. PMC 1378024. PMID 10762551. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1378024. 
  8. ^ Hamblin MT, Thompson EE, Di Rienzo A (February 2002). "Complex Signatures of Natural Selection at the Duffy Blood Group Locus". Am. J. Hum. Genet. 70 (2): 369–83. doi:10.1086/338628. PMC 419988. PMID 11753822. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=419988. 
  9. ^ Zimmerman PA, Woolley I, Masinde GL, Miller SM, McNamara DT, Hazlett F, Mgone CS, Alpers MP, Genton B, Boatin BA, Kazura JW (November 1999). "Emergence of FY*Anull in a Plasmodium vivax-endemic region of Papua New Guinea". Proc. Natl. Acad. Sci. U.S.A. 96 (24): 13973–7. Bibcode 1999PNAS...9613973Z. doi:10.1073/pnas.96.24.13973. PMC 24175. PMID 10570183. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=24175. 
  10. ^ Awasthi G, Dashb AP, Dasa A (September 2009). "Evolutionary insights into duffy gene in mammalian taxa with comparative genetic analysis". J Vector Borne Dis 46 (3): 230–6. PMID 19724088. 
  11. ^ Tung J, Primus A, Bouley AJ, Severson TF, Alberts SC, Wray GA (July 2009). "Evolution of a malaria resistance gene in wild primates". Nature 460 (7253): 388–91. Bibcode 2009Natur.460..388T. doi:10.1038/nature08149. PMID 19553936. 
  12. ^ a b Woolley IJ, Hotmire KA, Sramkoski RM, Zimmerman PA, Kazura JW (August 2000). "Differential expression of the duffy antigen receptor for chemokines according to RBC age and FY genotype". Transfusion 40 (8): 949–53. doi:10.1046/j.1537-2995.2000.40080949.x. PMID 10960522. 
  13. ^ Horuk R, Martin AW, Wang Z, et al. (1997). "Expression of chemokine receptors by subsets of neurons in the central nervous system". J. Immunol. 158 (6): 2882–90. PMID 9058825. 
  14. ^ Hadley TJ, Lu ZH, Wasniowska K,et al. (1994). "Postcapillary venule endothelial cells in kidney express a multispecific chemokine receptor that is structurally and functionally identical to the erythroid isoform, which is the Duffy blood group antigen". J. Clin. Invest. 94 (3): 985–91. doi:10.1172/JCI117465. PMC 295143. PMID 8083383. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=295143. 
  15. ^ Peiper SC, Wang ZX, Neote K, Martin AW, Showell HJ, Conklyn MJ, Ogborne K, Hadley TJ, Lu ZH, Hesselgesser J, Horuk R (April 1995). "The Duffy antigen/receptor for chemokines (DARC) is expressed in endothelial cells of Duffy negative individuals who lack the erythrocyte receptor". J. Exp. Med. 181 (4): 1311–7. doi:10.1084/jem.181.4.1311. PMC 2191961. PMID 7699323. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2191961. 
  16. ^ Chaudhuri A, Zbrzezna V, Polyakova J, Pogo AO, Hesselgesser J, Horuk R (1994). "Expression of the Duffy antigen in K562 cells. Evidence that it is the human erythrocyte chemokine receptor". J. Biol. Chem. 269 (11): 7835–8. PMID 8132497. 
  17. ^ Horuk R, Wang ZX, Peiper SC, Hesselgesser J (1994). "Identification and characterization of a promiscuous chemokine-binding protein in a human erythroleukemic cell line". J. Biol. Chem. 269 (26): 17730–3. PMID 7517400. 
  18. ^ Horuk R, Chitnis CE, Darbonne WC, Colby TJ, Rybicki A, Hadley TJ, Miller LH (August 1993). "A receptor for the malarial parasite Plasmodium vivax: the erythrocyte chemokine receptor". Science 261 (5125): 1182–4. Bibcode 1993Sci...261.1182H. doi:10.1126/science.7689250. PMID 7689250. http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=7689250. 
  19. ^ Lu ZH, Wang ZX, Horuk R, et al. (1995). "The promiscuous chemokine binding profile of the Duffy antigen/receptor for chemokines is primarily localized to sequences in the amino-terminal domain". J. Biol. Chem. 270 (44): 26239–45. doi:10.1074/jbc.270.44.26239. PMID 7592830. 
  20. ^ Chaudhuri A, Zbrzezna V, Polyakova J, Pogo AO, Hesselgesser J, Horuk R (March 1994). "Expression of the Duffy antigen in K562 cells. Evidence that it is the human erythrocyte chemokine receptor". J. Biol. Chem. 269 (11): 7835–8. PMID 8132497. 
  21. ^ Fukuma N, Akimitsu N, Hamamoto H, Kusuhara H, Sugiyama Y, Sekimizu K (2003). "A role of the Duffy antigen for the maintenance of plasma chemokine concentrations". Biochem. Biophys. Res. Commun. 303 (1): 137–9. doi:10.1016/S0006-291X(03)00293-6. PMID 12646177. 
  22. ^ a b Lee JS, Frevert CW, Wurfel MM, et al. (2003). "Duffy antigen facilitates movement of chemokine across the endothelium in vitro and promotes neutrophil transmigration in vitro and in vivo". J. Immunol. 170 (10): 5244–51. PMID 12734373. 
  23. ^ Dawson TC, Lentsch AB, Wang Z, et al. (2000). "Exaggerated response to endotoxin in mice lacking the Duffy antigen/receptor for chemokines (DARC)". Blood 96 (5): 1681–4. PMID 10961863. 
  24. ^ Patterson AM, Siddall H, Chamberlain G, Gardner L, Middleton J (2002). "Expression of the duffy antigen/receptor for chemokines (DARC) by the inflamed synovial endothelium". J. Pathol. 197 (1): 108–16. doi:10.1002/path.1100. PMID 12081195. 
  25. ^ Liu XH, Hadley TJ, Xu L, Peiper SC, Ray PE (1999). "Up-regulation of Duffy antigen receptor expression in children with renal disease". Kidney Int. 55 (4): 1491–500. doi:10.1046/j.1523-1755.1999.00385.x. PMID 10201015. 
  26. ^ Rot A (2005). "Contribution of Duffy antigen to chemokine function". Cytokine Growth Factor Rev. 16 (6): 687–94. doi:10.1016/j.cytogfr.2005.05.011. PMID 16054417. 
  27. ^ Segerer S, Regele H, MacK M, et al. (2000). "The Duffy antigen receptor for chemokines is up-regulated during acute renal transplant rejection and crescentic glomerulonephritis". Kidney Int. 58 (4): 1546–56. doi:10.1046/j.1523-1755.2000.00316.x. PMID 11012889. 
  28. ^ Segerer S, Cui Y, Eitner F, et al. (2001). "Expression of chemokines and chemokine receptors during human renal transplant rejection". Am. J. Kidney Dis. 37 (3): 518–31. doi:10.1016/S0272-6386(01)80009-3. PMID 11228176. 
  29. ^ Brühl H, Vielhauer V, Weiss M, Mack M, Schlöndorff D, Segerer S (2005). "Expression of DARC, CXCR3 and CCR5 in giant cell arteritis". Rheumatology (Oxford, England) 44 (3): 309–13. doi:10.1093/rheumatology/keh485. PMID 15572394. 
  30. ^ Middleton J, Americh L, Gayon R, et al. (2005). "A comparative study of endothelial cell markers expressed in chronically inflamed human tissues: MECA-79, Duffy antigen receptor for chemokines, von Willebrand factor, CD31, CD34, CD105 and CD146". J. Pathol. 206 (3): 260–8. doi:10.1002/path.1788. PMID 15887283. 
  31. ^ Segerer S, Böhmig GA, Exner M, et al. (2003). "When renal allografts turn DARC". Transplantation 75 (7): 1030–4. doi:10.1097/01.TP.0000054679.91112.6F. PMID 12698093. 
  32. ^ Pruenster M, Rot A (2006). "Throwing light on DARC". Biochem. Soc. Trans. 34 (Pt 6): 1005–8. doi:10.1042/BST0341005. PMID 17073738. 
  33. ^ Chakera A, Seeber RM, John AE, Eidne KA, Greaves DR (May 2008). "The duffy antigen/receptor for chemokines exists in an oligomeric form in living cells and functionally antagonizes CCR5 signaling through hetero-oligomerization". Mol. Pharmacol. 73 (5): 1362–70. doi:10.1124/mol.107.040915. PMID 18230715. 
  34. ^ Pruenster M, Mudde L, Bombosi P, Dimitrova S, Zsak M, Middleton J, Richmond A, Graham GJ, Segerer S, Nibbs RJ, Rot A (January 2009). "The Duffy antigen receptor for chemokines transports chemokines and supports their promigratory activity". Nat. Immunol. 10 (1): 101–8. doi:10.1038/ni.1675. PMID 19060902. 
  35. ^ Levinson, Warren (2004). Medical microbiology & immunology: examination & board review. New York: Lange Medical Books/McGraw-Hill. ISBN 0-07-143199-3. 
  36. ^ a b Nickel RG, Willadsen SA, Freidhoff LR, Huang SK, Caraballo L, Naidu RP, Levett P, Blumenthal M, Banks-Schlegel S, Bleecker E, Beaty T, Ober C, Barnes KC (August 1999). "Determination of Duffy genotypes in three populations of African descent using PCR and sequence-specific oligonucleotides". Hum. Immunol. 60 (8): 738–42. doi:10.1016/S0198-8859(99)00039-7. PMID 10439320. 
  37. ^ Miller LH, Mason SJ, Clyde DF, McGinniss MH (August 1976). "The resistance factor to Plasmodium vivax in blacks. The Duffy-blood-group genotype, FyFy". N. Engl. J. Med. 295 (6): 302–4. doi:10.1056/NEJM197608052950602. PMID 778616. 
  38. ^ Estalote AC, Proto-Siqueira R, Silva WA, Zago MA, Palatnik M (2005). "The mutation G298A-->Ala100Thr on the coding sequence of the Duffy antigen/chemokine receptor gene in non-caucasian Brazilians". Genet. Mol. Res. 4 (2): 166–73. PMID 16110438. http://www.funpecrp.com.br/gmr/year2005/vol2-4/gmr0122_abstract.htm. 
  39. ^ Bauduer F, Feingold J, Lacombe D (October 2005). "The Basques: review of population genetics and Mendelian disorders". Hum. Biol. 77 (5): 619–37. doi:10.1353/hub.2006.0001. PMID 16596943. 
  40. ^ Ferri G, Bini C, Ceccardi S, Ingravallo F, Lugaresi F, Pelotti S (March 2006). "Minisequencing-based genotyping of Duffy and ABO blood groups for forensic purposes". J. Forensic Sci. 51 (2): 357–60. doi:10.1111/j.1556-4029.2006.00058.x. PMID 16566771. 
  41. ^ Das MK, Singh SS, Adak T, Vasantha K, Mohanty D (June 2005). "The Duffy blood groups of Jarawas - the primitive and vanishing tribe of Andaman and Nicobar Islands of India". Transfus Med 15 (3): 237–40. doi:10.1111/j.1365-3148.2005.00583.x. PMID 15943709. 
  42. ^ Kobyliansky E, Micle S, Goldschmidt-Nathan M, Arensburg B, Nathan H (1980). "Duffy, Kell and P blood group systems in some Jewish populations of Israel". Acta Anthropogenet 4 (3–4): 173–9. PMID 7346047. 
  43. ^ Parasol N, Cohen N, Zemishlany Z, Lerer B, Kosower NS (April 2001). "Duffy antigen/receptor for chemokines (DARC): genotypes in Ashkenazi and non-Ashkenazi Jews in Israel". Hum. Biol. 73 (2): 307–13. doi:10.1353/hub.2001.0024. PMID 11446431. 
  44. ^ Yan L, Zhu F, Fu Q, He J (2005). "ABO, Rh, MNS, Duffy, Kidd,Yt, Scianna, and Colton blood group systems in indigenous Chinese". Immunohematology 21 (1): 10–4. PMID 15783300. 
  45. ^ Chiaroni J, Touinssi M, Frassati C, Degioanni A, Gibert M, Reviron D, Mercier P, Boëtsch G (August 2004). "Genetic characterization of the population of Grande Comore Island (Njazidja) according to major blood groups". Hum. Biol. 76 (4): 527–41. doi:10.1353/hub.2004.0053. PMID 15754970. 
  46. ^ Sellami MH, Kaabi H, Midouni B, Dridi A, Mojaat N, Boukef MK, Hmida S (2008). "Duffy blood group system genotyping in an urban Tunisian population". Ann. Hum. Biol. 35 (4): 406–15. doi:10.1080/03014460802082127. PMID 18608113. 
  47. ^ Thakral B, Saluja K, Sharma RR, Marwaha N (June 2010). "Phenotype frequencies of blood group systems (Rh, Kell, Kidd, Duffy, MNS, P, Lewis, and Lutheran) in north Indian blood donors". Transfus Apher Sci 43 (1): 17–22. doi:10.1016/j.transci.2010.05.006. PMID 20558108. 
  48. ^ Lepers JP, Simonneau M, Charmot G (1986). "[The Duffy blood group system in the population of Nouakchott (Mauritania)]" (in French). Bull Soc Pathol Exot Filiales 79 (3): 417–20. PMID 3769126. 
  49. ^ Howes RE, Patil AP, Piel FB, Nyangiri OA, Kabaria CW, Gething PW, Zimmerman PA, Barnadas C, Beall CM, Gebremedhin A, Ménard D, Williams TN, Weatherall DJ, Hay SI (April 2011). "The global distribution of the Duffy blood group". Nat Commun 2 (4): 266. Bibcode 2011NatCo...2E.266H. doi:10.1038/ncomms1265. PMC 3074097. PMID 21468018. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3074097. 
  50. ^ Vergara C, Tsai YJ, Grant AV, Rafaels N, Gao L, Hand T, Stockton M, Campbell M, Mercado D, Faruque M, Dunston G, Beaty TH, Oliveira RR, Ponte EV, Cruz AA, Carvalho E, Araujo MI, Watson H, Schleimer RP, Caraballo L, Nickel RG, Mathias RA, Barnes KC (November 2008). "Gene Encoding Duffy Antigen/Receptor for Chemokines Is Associated with Asthma and IgE in Three Populations". Am. J. Respir. Crit. Care Med. 178 (10): 1017–22. doi:10.1164/rccm.200801-182OC. PMC 2582596. PMID 18827265. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2582596. 
  51. ^ Reich D, Nalls MA, Kao WH, Akylbekova EL, Tandon A, Patterson N, Mullikin J, Hsueh WC, Cheng CY, Coresh J, Boerwinkle E, Li M, Waliszewska A, Neubauer J, Li R, Leak TS, Ekunwe L, Files JC, Hardy CL, Zmuda JM, Taylor HA, Ziv E, Harris TB, Wilson JG (January 2009). Visscher, Peter M.. ed. "Reduced Neutrophil Count in People of African Descent Is Due To a Regulatory Variant in the Duffy Antigen Receptor for Chemokines Gene". PLoS Genet. 5 (1): e1000360. doi:10.1371/journal.pgen.1000360. PMC 2628742. PMID 19180233. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2628742. 
  52. ^ Zijlstra A, Quigley JP (September 2006). "The DARC side of metastasis: shining a light on KAI1-mediated metastasis suppression in the vascular tunnel". Cancer Cell 10 (3): 177–8. doi:10.1016/j.ccr.2006.08.012. PMID 16959609. 
  53. ^ Wang J, Ou ZL, Hou YF, Luo JM, Shen ZZ, Ding J, Shao ZM (November 2006). "Enhanced expression of Duffy antigen receptor for chemokines by breast cancer cells attenuates growth and metastasis potential". Oncogene 25 (54): 7201–11. doi:10.1038/sj.onc.1209703. PMID 16785997. 
  54. ^ Mayr FB, Spiel AO, Leitner JM, Firbas C, Jilma-Stohlawetz P, Chang JY, Key NS, Jilma B (April 2009). "Racial differences in endotoxin-induced tissue factor-triggered coagulation". J. Thromb. Haemost. 7 (4): 634–40. doi:10.1111/j.1538-7836.2009.03307.x. PMID 19187081. 
  55. ^ a b He W, Neil S, Kulkarni H, Wright E, Agan BK, Marconi VC, Dolan MJ, Weiss RA, Ahuja SK (July 2008). "Duffy Antigen Receptor for Chemokines Mediates trans-Infection of HIV-1 from Red Blood Cells to Target Cells and Affects HIV-AIDS Susceptibility". Cell Host Microbe 4 (1): 52–62. doi:10.1016/j.chom.2008.06.002. PMC 2562426. PMID 18621010. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2562426. 
  56. ^ Kulkarni H, Marconi VC, He W, Landrum ML, Okulicz JF, Delmar J, Kazandjian D, Castiblanco J, Ahuja SS, Wright EJ, Weiss RA, Clark RA, Dolan MJ, Ahuja SK (July 2009). "The Duffy-null state is associated with a survival advantage in leukopenic HIV-infected persons of African ancestry". Blood 114 (13): 2783–92. doi:10.1182/blood-2009-04-215186. PMC 2927046. PMID 19620399. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2927046. 
  57. ^ Ramsuran V, Kulkarni H, He W, Mlisana K, Wright EJ, Werner L, Castiblanco J, Dhanda R, Le T, Dolan MJ, Guan W, Weiss RA, Clark RA, Abdool Karim SS, Ahuja SK, Ndung'u T (May 2011). "Duffy-Null–Associated Low Neutrophil Counts Influence HIV-1 Susceptibility in High-Risk South African Black Women". Clin. Infect. Dis. 52 (10): 1248–56. doi:10.1093/cid/cir119. PMC 3115278. PMID 21507922. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3115278. 
  58. ^ Geleff S, Draganovici D, Jaksch P, Segerer S (July 2009). "The role of chemokine receptors in acute lung allograft rejection". Eur. Respir. J. 35 (1): 167–75. doi:10.1183/09031936.00042309. PMID 19608592. 
  59. ^ a b c Ryan JR, Stoute JA, Amon J, Dunton RF, Mtalib R, Koros J, Owour B, Luckhart S, Wirtz RA, Barnwell JW, Rosenberg R (October 2006). "Evidence for transmission of Plasmodium vivax among a duffy antigen negative population in Western Kenya". Am. J. Trop. Med. Hyg. 75 (4): 575–81. doi:10.1056/NEJM197608052950602. PMID 17038676. 
  60. ^ Ménard D, Barnadas C, Bouchier C, Henry-Halldin C, Gray LR, Ratsimbasoa A, Thonier V, Carod JF, Domarle O, Colin Y, Bertrand O, Picot J, King CL, Grimberg BT, Mercereau-Puijalon O, Zimmerman PA (March 2010). "Plasmodium vivax clinical malaria is commonly observed in Duffy-negative Malagasy people". Proc. Natl. Acad. Sci. U.S.A. 107 (13): 5967–71. Bibcode 2010PNAS..107.5967M. doi:10.1073/pnas.0912496107. PMC 2851935. PMID 20231434. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2851935. 
  61. ^ Mendes C, Dias F, Figueiredo J, Mora VG, Cano J, de Sousa B, do Rosário VE, Benito A, Berzosa P, Arez AP (June 2011). Franco-Paredes, Carlos. ed. "Duffy Negative Antigen Is No Longer a Barrier to Plasmodium vivax – Molecular Evidences from the African West Coast (Angola and Equatorial Guinea)". PLoS Negl Trop Dis 5 (6): e1192. doi:10.1371/journal.pntd.0001192. PMC 3119644. PMID 21713024. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3119644. 
  62. ^ Wurtz N, Lekweiry Mint K, Bogreau H, Pradines B, Rogier C, Salem Boukhary AO, Hafid JE, Ahmedou Salem MS, Trape JF, Basco LK, Briolant S (2011) Vivax malaria in Mauritania includes infection of a Duffy-negative individual. Malar J 10(1):336.
  63. ^ Cavasini CE, de Mattos LC, Couto AA, Couto VS, Gollino Y, Moretti LJ, Bonini-Domingos CR, Rossit AR, Castilho L, Machado RL (2007). "Duffy blood group gene polymorphisms among malaria vivax patients in four areas of the Brazilian Amazon region". Malar. J. 6: 167. doi:10.1186/1475-2875-6-167. PMC 2244634. PMID 18093292. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2244634. 
  64. ^ Cavasini CE, Mattos LC, Couto AA, Bonini-Domingos CR, Valencia SH, Neiras WC, Alves RT, Rossit AR, Castilho L, Machado RL (October 2007). "Plasmodium vivax infection among Duffy antigen-negative individuals from the Brazilian Amazon region: an exception?". Trans. R. Soc. Trop. Med. Hyg. 101 (10): 1042–4. doi:10.1016/j.trstmh.2007.04.011. PMID 17604067. 
  65. ^ McHenry AM, Barnwell JW, Adams JH (October 2009). "Plasmodium vivax DBP binding to Aotus nancymaae erythrocytes is Duffy antigen dependent". J. Parasitol. 96 (1): 1–7. doi:10.1645/GE-2281.1. PMC 2883003. PMID 19799492. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2883003. 
  66. ^ Albuquerque SR, de Oliveira Cavalcante F, Sanguino EC, Tezza L, Chacon F, Castilho L, Dos Santos MC (February 2010). "FY polymorphisms and vivax malaria in inhabitants of Amazonas State, Brazil". Parasitol Res 106 (5): 1049–53. doi:10.1007/s00436-010-1745-x. PMID 20162434. 
  67. ^ Guler N, Turgut M, Ozatli D, Turgut Y, Gokce AK, Koc S, Albayrak D (March 2009). "High ratio of Duffy (a+b+) phenotype in patients with multiple myeloma compared to healthy controls". Hematol Oncol 27 (1): 50–1. doi:10.1002/hon.887. PMID 19206111. 
  68. ^ Elson JK, Beebe-Dimmer JL, Morgenstern H, Chilkuri M, Blanchard J, Lentsch AB (July 2010). "The Duffy Antigen/Receptor for Chemokines (DARC) and Prostate-Cancer Risk among Jamaican Men". J Immigr Minor Health 13 (1): 36–41. doi:10.1007/s10903-010-9330-z. PMC 3017736. PMID 20596779. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3017736. 
  69. ^ Watorek E, Boratyńska M, Hałoń A, Klinger M (2008). "Anti-Fya antibodies as the cause of an unfortunate post-transplant course in renal transplant recipient". Ann. Transplant. 13 (1): 48–52. PMID 18344944. 
  70. ^ Afenyi-Annan A, Kail M, Combs MR, Orringer EP, Ashley-Koch A, Telen MJ (May 2008). "Lack of Duffy antigen expression is associated with organ damage in patients with sickle cell disease". Transfusion 48 (5): 917–24. doi:10.1111/j.1537-2995.2007.01622.x. PMID 18248572. 
  71. ^ Nebor D, Durpes MC, Mougenel D, Mukisi-Mukaza M, Elion J, Hardy-Dessources MD, Romana M (July 2010). "Association between Duffy antigen receptor for chemokines expression and levels of inflammation markers in sickle cell anemia patients". Clin. Immunol. 136 (1): 116–22. doi:10.1016/j.clim.2010.02.023. PMID 20347396. 
  72. ^ Woolley IJ, Hutchinson P, Reeder JC, Kazura JW, Cortés A (2009). "Southeast Asian ovalocytosis is associated with increased expression of Duffy antigen receptor for chemokines (DARC)". Immunohematology 25 (2): 63–6. PMID 19927622. 

Further reading

  • Pogo AO, Chaudhuri A (1996). "Duffy and receptors for P. vivax and chemotactic peptides". Transfusion clinique et biologique : journal de la Société française de transfusion sanguine 2 (4): 269–76. PMID 8542025. 
  • Pruenster M, Rot A (2007). "Throwing light on DARC". Biochem. Soc. Trans. 34 (Pt 6): 1005–8. doi:10.1042/BST0341005. PMID 17073738. 
  • Raeymaekers P, Van Broeckhoven C, Backhovens H, et al. (1988). "The Duffy blood group is linked to the alpha-spectrin locus in a large pedigree with autosomal dominant inheritance of Charcot-Marie-Tooth disease type 1". Hum. Genet. 78 (1): 76–8. doi:10.1007/BF00291239. PMID 2892777. 
  • Lu ZH, Wang ZX, Horuk R, et al. (1995). "The promiscuous chemokine binding profile of the Duffy antigen/receptor for chemokines is primarily localized to sequences in the amino-terminal domain". J. Biol. Chem. 270 (44): 26239–45. doi:10.1074/jbc.270.44.26239. PMID 7592830. 
  • Horuk R, Chitnis CE, Darbonne WC, et al. (1993). "A receptor for the malarial parasite Plasmodium vivax: the erythrocyte chemokine receptor". Science 261 (5125): 1182–4. Bibcode 1993Sci...261.1182H. doi:10.1126/science.7689250. PMID 7689250. 
  • Tournamille C, Le Van Kim C, Gane P, et al. (1995). "Molecular basis and PCR-DNA typing of the Fya/fyb blood group polymorphism". Hum. Genet. 95 (4): 407–10. doi:10.1007/BF00208965. PMID 7705836. 
  • Iwamoto S, Omi T, Kajii E, Ikemoto S (1995). "Genomic organization of the glycoprotein D gene: Duffy blood group Fya/Fyb alloantigen system is associated with a polymorphism at the 44-amino acid residue". Blood 85 (3): 622–6. PMID 7833467. 
  • Horuk R, Martin AW, Wang Z, et al. (1997). "Expression of chemokine receptors by subsets of neurons in the central nervous system". J. Immunol. 158 (6): 2882–90. PMID 9058825. 
  • Tournamille C, Le Van Kim C, Gane P, et al. (1997). "Close association of the first and fourth extracellular domains of the Duffy antigen/receptor for chemokines by a disulfide bond is required for ligand binding". J. Biol. Chem. 272 (26): 16274–80. doi:10.1074/jbc.272.26.16274. PMID 9195930. 
  • Tournamille C, Le Van Kim C, Gane P, et al. (1998). "Arg89Cys substitution results in very low membrane expression of the Duffy antigen/receptor for chemokines in Fy(x) individuals". Blood 92 (6): 2147–56. PMID 9731074. 
  • Parasol N, Reid M, Rios M, et al. (1998). "A novel mutation in the coding sequence of the FY*B allele of the Duffy chemokine receptor gene is associated with an altered erythrocyte phenotype". Blood 92 (7): 2237–43. PMID 9746760. 
  • Olsson ML, Smythe JS, Hansson C, et al. (1999). "The Fy(x) phenotype is associated with a missense mutation in the Fy(b) allele predicting Arg89Cys in the Duffy glycoprotein". Br. J. Haematol. 103 (4): 1184–91. doi:10.1046/j.1365-2141.1998.01083.x. PMID 9886340. 
  • Lachgar A, Jaureguiberry G, Le Buenac H, et al. (1999). "Binding of HIV-1 to RBCs involves the Duffy antigen receptors for chemokines (DARC)". Biomed. Pharmacother. 52 (10): 436–9. doi:10.1016/S0753-3322(99)80021-3. PMID 9921412. 
  • Zimmerman PA, Woolley I, Masinde GL, et al. (2000). "Emergence of FY*Anull in a Plasmodium vivax-endemic region of Papua New Guinea". Proc. Natl. Acad. Sci. U.S.A. 96 (24): 13973–7. Bibcode 1999PNAS...9613973Z. doi:10.1073/pnas.96.24.13973. PMC 24175. PMID 10570183. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=24175. 
  • Woolley IJ, Kalayjian R, Valdez H, et al. (2002). "HIV nephropathy and the Duffy antigen/receptor for Chemokines in African Americans". J. Nephrol. 14 (5): 384–7. PMID 11730271. 
  • Hamblin MT, Thompson EE, Di Rienzo A (2002). "Complex Signatures of Natural Selection at the Duffy Blood Group Locus". Am. J. Hum. Genet. 70 (2): 369–83. doi:10.1086/338628. PMC 419988. PMID 11753822. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=419988. 
  • Patterson AM, Siddall H, Chamberlain G, et al. (2002). "Expression of the duffy antigen/receptor for chemokines (DARC) by the inflamed synovial endothelium". J. Pathol. 197 (1): 108–16. doi:10.1002/path.1100. PMID 12081195. 

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