TLR-2 is a biomolecule, which plays a role in the human immune system. TLR-2 is a membrane protein, a receptor, which is expressed on the surface of certain cells and recognizes native or foreign substances, and passes on appropriate signals to the cell and/or the nervous system.

TLR-2 is a member of a large family of homologous Toll-like receptors (TLRs). TLR2 has also been designated as CD282 (cluster of differentiation 282).


TLR-2 is a membrane receptor found at the surface of immune system cells that recognises many bacterial, fungal, viral and endogenous substances. Phagocytosis of bound materials takes place in endosome/phagosome and a cellular activation, so that the elements of the innate immune system take over such as macrophages, PMN and dendritic cells tasks of the nonspecific immune defense, B1a and form MZB first anti-bodies and uses in the process the specific anti-body formation. Here cytokine is involved e.g. Tumor necrosis factor-alpha (TNF α) and different interleukins (IL-1alpha, IL-1beta, IL-6, IL-8, IL-12). Before TLRs were discovered, some of the materials specified below were grouped under the term so-called "Moduline". By that rather Th1 appropriate cytokine pattern is seen in most experimental models an immune deviation this way, away of the Th2-expression. Conjugates are developed as vaccines or already used without a priori knowledge.

One only 2006 recognized characteristic is the expression of the TLR-2 on the Tregs (special form of the T-cells), which is brought equally to TCR determined proliferation and functional inactivity. Thereby, a disinhibition of the early inflammation phase and the specific anti-body formation is reached. After reduction of the exciter number many exciter-specific Tregs are present, which, now without TLR-2-Signal, become active and the specific like the inflammatory immune reaction to restrain (see also TGF beta, Interleukin 10). Older literature, which attributes a direct immune stimulation effect over TLR-2 to a given substance, must be interpreted under circumstances that the used TLR-2-knockouts has regularly quite few Tregs.

Functionally relevant polymorphism is described, which reduced to a function restriction and thus usually survival rate with infections/sepsis with Gram-positive bacteria leads in particular.

The signal transduction is represented in the article toll-like receptor.


TLR-2 is expressed on microglia, Schwann cells, monocytes, macrophages, dendritic cells, polymorphonuclear leukocytes, B-cells (B1a, MZB, B2), T-cells including regulatory T cells (CD4, CD25). TLR-2 is likewise in the epithelium of the bronchial tube and the alveoli.


Further reading

citations =
*cite journal | author=Aderem A, Ulevitch RJ |title=Toll-like receptors in the induction of the innate immune response. |journal=Nature |volume=406 |issue= 6797 |pages= 782–7 |year= 2000 |pmid= 10963608 |doi= 10.1038/35021228
*cite journal | author=Muzio M, Polentarutti N, Bosisio D, "et al." |title=Toll-like receptor family and signalling pathway. |journal=Biochem. Soc. Trans. |volume=28 |issue= 5 |pages= 563–6 |year= 2001 |pmid= 11044375 |doi=
*cite journal | author=Hallman M, Rämet M, Ezekowitz RA |title=Toll-like receptors as sensors of pathogens. |journal=Pediatr. Res. |volume=50 |issue= 3 |pages= 315–21 |year= 2002 |pmid= 11518816 |doi=
*cite journal | author=Dziarski R, Gupta D |title=Role of MD-2 in TLR2- and TLR4-mediated recognition of Gram-negative and Gram-positive bacteria and activation of chemokine genes. |journal=J. Endotoxin Res. |volume=6 |issue= 5 |pages= 401–5 |year= 2001 |pmid= 11521063 |doi=
*cite journal | author=Lien E, Ingalls RR |title=Toll-like receptors. |journal=Crit. Care Med. |volume=30 |issue= 1 Suppl |pages= S1–11 |year= 2002 |pmid= 11782555 |doi=
*cite journal | author=Xu D, Komai-Koma M, Liew FY |title=Expression and function of Toll-like receptor on T cells. |journal=Cell. Immunol. |volume=233 |issue= 2 |pages= 85–9 |year= 2005 |pmid= 15950961 |doi= 10.1016/j.cellimm.2005.04.019
*cite journal | author=Lorenz E |title=TLR2 and TLR4 expression during bacterial infections. |journal=Curr. Pharm. Des. |volume=12 |issue= 32 |pages= 4185–93 |year= 2007 |pmid= 17100621 |doi=

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