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EDITORIAL article

Front. Immunol.
Sec. Molecular Innate Immunity
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1505715
This article is part of the Research Topic Community Series in The Role of Toll-like Receptors and their Related Signaling Pathways in Viral Infection and Inflammation: Volume II View all 5 articles

Research Topic: The Role of Toll-like Receptors and their Related Signaling Pathways in Viral Infection and Inflammation

Provisionally accepted
Ralf Kircheis Ralf Kircheis 1*Oliver Planz Oliver Planz 2*
  • 1 Syntacoll GmbH, Saal an der Donau, Germany
  • 2 University of Tübingen, Tübingen, Baden-Württemberg, Germany

The final, formatted version of the article will be published soon.

    Editorial The second volume of our Community Series on "The Role of Toll-like Receptors and their Related Signaling Pathways in Viral Infection and Inflammation" delves into the intricate mechanisms through which TLRs influence the immune response against viral pathogens. This collection, led by diverse researchers, expands our understanding of TLRs and their role in inflammation. Included studies comprehensively examine how TLR activation regulates different stages of inflammation. For example, research by Butcher et al. highlights macrophage tolerance in TLR signaling, crucial for adapting to chronic endotoxin exposure and mitigating prolonged pro-inflammatory cytokine production. This adaptation aims to protect host tissues from damage, observed across various TLR ligands, particularly TLR4's ligand lipopolysaccharide (LPS), which induces global shifts towards anti-inflammatory responses https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2018.00933/full. Additionally, Ricci-Azevedo et al. discuss lectins as TLR agonists with immunomodulatory properties. Plant lectin ArtinM and microbial lectins interact with TLR2 and TLR4, triggering NF-κB activation and IL-12 production in vitro. In vivo studies show these lectins confer resistance to intracellular pathogens. Lectins from pathogens like Toxoplasma gondii and Paracoccidioides brasiliensis also activate TLRs, suggesting potential for new pharmaceutical tools against infections and tumors https://www.frontiersin.org/articles/10.3389/fimmu.2017.01820. Moreover, Lu et al.'s review underscores TLRs' significant role in inflammatory bowel disease (IBD), a chronic global condition. Dysfunctions in TLR-mediated pathways contribute to IBD pathogenesis and influence treatment efficacy, prompting exploration of novel therapeutic strategies https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2018.00072/full. Lastly, Popotas et al. explore sex-specific immune responses in acute inflammatory diseases, attributing these differences to genes on the X chromosome encoding TLRs. Their review highlights distinct inflammatory patterns between sexes, crucial for tailoring clinical approaches https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1379754/full. This volume aims to advance our understanding of TLRs in inflammation, driving targeted therapy development and improving patient outcomes. We extend gratitude to all contributors for their invaluable insights and dedication to this critical field.

    Keywords: Toll-like receptor, Signalling pathway, viral infection, Inflammation, tolerance

    Received: 03 Oct 2024; Accepted: 07 Oct 2024.

    Copyright: © 2024 Kircheis and Planz. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Ralf Kircheis, Syntacoll GmbH, Saal an der Donau, Germany
    Oliver Planz, University of Tübingen, Tübingen, 72074, Baden-Württemberg, Germany

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.