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Redundant and regulatory roles for TLRs in Leishmania infection.

Redundant and regulatory roles for TLRs in Leishmania infection.
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Chauhan P, Shukla D, Chattopadhyay D, Saha B,


Chauhan P, Shukla D, Chattopadhyay D, Saha B, (click to view)

Chauhan P, Shukla D, Chattopadhyay D, Saha B,

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Clinical and experimental immunology 2017 07 14() doi 10.1111/cei.13014

Abstract

Toll-like receptors (TLRs) are germ-line encoded, non-clonal innate immune receptors, which are often the first receptors to recognize the molecular patterns on pathogens. Therefore, the immune response initiated by TLRs does have far-reaching consequences on the outcome of an infection. As soon as the cell surface TLRs and other receptors recognize a pathogen, the pathogen is phagocytosed. Inclusion of TLRs in the phagosome results in quicker phagosomal maturation and stronger adaptive immune response, as TLRs influence costimulatory molecules expression and determinant selection by MHC class-II and by MHC class-I for cross-presentation. The signals delivered by the TCR-peptide-MHC complex and the costimulatory molecules are indispensable for optimal T cell activation. In addition, the cytokines induced by TLRs can skew the differentiation of activated T cells to different effector T cell subsets. However, the potential of TLRs to influence adaptive immune response into different patterns is severely restricted by multiple factors: gross specificity for the molecular patterns, lack of receptor rearrangements, sharing of limited number of adaptors that assemble signaling complexes and redundancy in ligand recognition. These features of apparent redundancy and regulation in the functioning of TLRs characterize them as important and probable contributory factor in the resistance or susceptibility to an infection. This article is protected by copyright. All rights reserved.

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