TLR2 but not mediates responses elicited by components of  such as peptidoglycan and lipoteichoic acid. TLR2 recognizes acylated outer membrane lipoporteins of Gram-positive bacteria. TLR2, often with the collaboration of TLR6, binds a wide variety of molecular classes found in microbes, including peptidoglycans, zymosans and bacterial lipoptides. One of the best characterized TLR2 ligands is Staphylococcus aureus (gram-positive bacteria) lipoteichoic acid (LTA) TLR2 stimulation by bacterial lipoproteins results in only low levels of IL12p70 in monocyte derived DCs, but increases the expression of the p40 and p19 subunits of IL23, which induces a Th1 type immune response.

TLR2 recognizes diacyl and tracyl lipids. Where recognizes Hexacyl lipids such as found on LPS.

In mouse macrophages, two NF-kB binding sites of mTLR2 promoter are essential for the transcriptional responde to TNf-alpha. They are also important for the LPS response, but transcriptional factors other than NF-kB are also activated by LPS.

TLR uses TIRAP and MyD88 but not TRIF in signalling.

Regulation of TLR2 mRNA and Protein Expression 

Regulatory roles of activation pathways in the regulation of TLR2 mRNA vary considerably in different cell types. Although LPS is known to activate varous MAP kinase pathways, the activaiton of ERK, p38 kinase or JNK does not seem to be essential for the induction of TLR2 gene expression RAW264.7 cells. PD98059, a specific inhibitor of ERK pathway, rather enhances TLR2 mRNA increase by LPS, suggesting that ERK activaiton has an inhibitory effect on TLR2 expression in macrophages. Anisomycin, a potent activator of both UJNK and p38 MAP inase fail to induce TLR2 mRNA, suggesting that these MAP kinases are not sufficient for TLR2 gene up-regulation. Additionally, SB208530, a specific inhibitor of the p38 MAP inase pathway, was only slightly inhibitory to LPS mediated TLR2 induction.

Roll of TLR induction 

In response to gram-negative bacteria in macrophages, it has been suggested that at the initial stage of infection, LPS signals are mediated by the constitutively expressed TLR4 in combination with CD14. LPS signals and signals from the secreted cytokines (such as TNF-alpha and IL-1beta) then lead to the induction of TLR2 expression. Induced TLR2 mediates signals from other bacterial components and LPS leading to accelerated immune responses.