Mouse TLR2 Antibody

Toll-Like receptors (TLRs) play a critical role in early innate immunity to invading pathogens by sensing microorganisms. These evolutionarily conserved receptors recognize highly conserved structural motifs only expressed by microbial pathogens, called pathogen-associated microbial patterns (PAMPs). Stimulation of TLRs by PAMPs initiates a signaling cascade leading to the secretion of proinflammatory cytokines following NF-κB activation. To date ten human and twelve murine TLRs have been characterized, TLR1 to TLR10 in humans, TLR1 to TLR9, TLR11, TLR12 (aka TLR11), and TLR13 in mice, the homolog of TLR10 being a pseudogene.

TLR2 is involved in the recognition of a wide array of microbial molecules. TLR2 recognizes lipoteichoic acid and lipoprotein from gram-positive bacteria, lipoarabinomannan from mycobacteria, and zymosan from yeast cell wall. Moreover, TLR2 participates in the recognition of some types of LPS. TLR2 is known to heterodimerize with other TLRs, a property believed to extend the range of microbial molecules that TLR2 can recognize. TLR2 cooperates with TLR6 in response to diacylated mycoplasmal lipopeptides [1], and associates with TLR1 to recognize triacylated lipopeptides [2]. Furthermore, pathogen recognition by TLR2 is strongly enhanced by CD14 [3].

1. Girard R et al., 2003. Lipopolysaccharides from Legionella and Rhizobium stimulate mouse bone marrow granulocytes via Toll-like receptor 2. J Cell Sci. 116(Pt 2):293-302.
2. Ozinsky A. et al., 2000. The repertoire for pattern recognition of pathogens by the innate immune system is defined by cooperation between toll-like receptors. Proc Natl Acad Sci USA. 97(25):13766-71.
3. Lotz S. et al., 2004. Highly purified lipoteichoic acid activates neutrophil granulocytes and delays their spontaneous apoptosis via CD14 and TLR2. J Leukoc Biol. 75(3):467-77.