Toll-like receptors (TLRs) comprise a major family of pattern-recognition receptors (PRRs)
that fulfill a key role in recognizing, discriminating and responding appropriately to microbial infection.
Although expressed principally by macrophages and dendritic cells, TLRs expression is widespread and
includes, but is not limited to cells of myeloid and lymphoid origin. Activation of TLRs by their
cognate ligands can lead to induction of proinflammatory cytokine and antimicrobial peptide expression
or up regulation of type 1 interferons. Whilst central to innate immunity, TLRs can additionally
communicate with the adaptive immune response via modulation of cell-adhesion and co-stimulatory
molecules to induce longer term immunity. Interestingly a selection of non-microbial endogenous
factors can also activate certain TLRs, with dysregulation of these events having potentially deleterious
consequences. Since the first report of human TLR4 by Medzhitov and Janeway in 1997 [1] there has
been huge progress in elucidating the fundamental processes controlling the biology of the TLR family.
Keywords: TLRs, PAMPs, DAMPs, MyD88-dependent, TRIF-dependent signaling.
