Abstract

Toll like receptors (TLRs) function as pattern-recognition receptors (PRRs) and play key roles in the recognition of microbial components or endogenous ligands induced during inflammatory response. Studies on TLR-deficient mice have indicated TLRs' involvement in multiple pathologic conditions, and targeting of either the TLRs themselves or the signals they generate is proving to be of great interest to researchers as evidenced by increased research findings among immunologists, pharmacologist, and pharmaceutical scientists on TLRs. As animal models, cellular and molecular mechanisms on TLR mediated disease pathogenesis are made available, drug intervention strategies and early stage clinical studies can be planned and initiated to seek clinical proof for justifying TLRs and their associated signaling pathway/molecules as therapeutic targets. Moreover, a key functional output from TLRs is the generation of inflammatory cytokines such as tumor necrosis factor (TNF) and IL-6, which are excellent targets for inflammatory diseases such as rheumatoid arthritis.

Key words: TLR, PRR, NF-κB, agonist, antagonist, drug discovery.