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Abstract
<p class="first" id="d8934022e75">Immunopolymorphism is considered as an important
aspect behind the resistance or susceptibility
of the host to an infectious disease. Over the years, researchers have explored many
genetic factors for their role in immune surveillance against infectious diseases.
Polymorphic characters in the gene encoding Toll-like receptors (TLRs) play profound
roles in inducing differential immune responses by the host against parasitic infections.
Protein(s) encoded by TLR gene(s) are immensely important due to their ability of
recognizing different types of pathogen associated molecular patterns (PAMPs). This
study reviews the polymorphic residues present in the nucleotide or in the amino acid
sequence of TLRs and their influence on alteration of inflammatory signalling pathways
promoting either susceptibility or resistance to major infectious diseases, including
tuberculosis, leishmaniasis, malaria and filariasis. Population-based studies exploring
TLR polymorphisms in humans are primarily emphasized to discuss the association of
the polymorphic residues with the occurrence and epidemiology of the mentioned infectious
diseases. Principal polymorphic residues in TLRs influencing immunity to infection
are mostly single nucleotide polymorphisms (SNPs). I602S (TLR1), R677W (TLR2), P554S
(TLR3), D299G (TLR4), F616L (TLR5), S249P (TLR6), Q11L (TLR7), M1V (TLR8), G1174A
(TLR9) and G1031T (TLR10) are presented as the major influential SNPs in shaping immunity
to pathogenic infections. The contribution of these SNPs in the structure-function
relationship of TLRs is yet not clear. Therefore, molecular studies on such polymorphisms
can improve our understanding on the genetic basis of the immune response and pave
the way for therapeutic intervention in a more feasible way.
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