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Insights into the toll-like receptors in sexually transmitted infections

Research output: Contribution to journalReviewResearchpeer-review

DOI

  1. Involvement of NLRP3 and NLRC4 Inflammasome in Uropathogenic E. coli Mediated Urinary Tract Infections

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Inflammasomes and Their Role in Innate Immunity of Sexually Transmitted Infections

    Research output: Contribution to journalReviewResearchpeer-review

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Toll-like receptors (TLRs) are like soldiers of an innate immune system, which protects vital biological processes against invading pathogens. TLR signalling pathways help in the removal of pathogens and mediate well-established inflammatory processes. However, these processes may also aid in the development or augmentation of an infection or an autoimmune disease. Recent studies have delineated TLR polymorphism's role in the loss of function, making hosts more resistant or vulnerable to the development of an infection. In this review, we have discussed the association of TLRs with sexually transmitted infections (STIs), especially to the pathogen-specific ligands. We have also assessed the impact on TLR downstream signalling and the maintenance of cellular homeostasis during immune responses. Besides, we have discussed the role of TLRs single nucleotide polymorphisms in various STIs. Since TLRs are known to play a part in defence mechanisms and in aiding infections therefore, a thorough understanding of TLRs structure and molecular mechanisms is required to explain how they can influence the outcome of an STI. Such a strategy may lead to the development of novel and useful immunotherapeutic approaches to control pathogen progression and prevent transmission.

Original languageEnglish
JournalScandinavian Journal of Immunology
Volume93
Issue number1
Pages (from-to)e12954
ISSN0300-9475
DOIs
Publication statusPublished - Jan 2020

    Research areas

  • Adaptive Immunity, Animals, Disease Susceptibility, Genetic Predisposition to Disease, Host-Pathogen Interactions, Humans, Immunity, Innate, Polymorphism, Single Nucleotide, Sexually Transmitted Diseases/diagnosis, Signal Transduction, Toll-Like Receptors/genetics

ID: 62331766