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REVIEW article

Front. Immunol.
Sec. Mucosal Immunity
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1446072
This article is part of the Research Topic The Synthesis of Secretory Immunoglobulin A in Mucosal Tissue: Mucosal-associated Invariant T, T Follicular Helper, and B Cells View all 4 articles

Role of cellular effectors in the induction and maintenance of IgA responses leading to protective immunity against enteric bacterial pathogens

Provisionally accepted
Laura E. Carreto-Binaghi Laura E. Carreto-Binaghi 1,2,3Marcelo B. Sztein Marcelo B. Sztein 1,2,4,5*Jayaum S. Booth Jayaum S. Booth 1,2*
  • 1 Center for Vaccine Development, School of Medicine, University of Maryland, Baltimore, United States
  • 2 Department of Pediatrics, University of Maryland School of Medicine, Baltimore, Maryland, United States
  • 3 National Institute of Respiratory Diseases-Mexico (INER), Mexico City, Mexico
  • 4 Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, United States
  • 5 Tumor Immunology and Immunotherapy Program, University of Maryland Marlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore, United States

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

    The mucosal immune system is a critical first line of defense to infectious diseases, as many pathogens enter the body through mucosal surfaces, disrupting the balanced interactions between mucosal cells, secretory molecules, and microbiota in this challenging microenvironment. The mucosal immune system comprises a complex and integrated network that includes the gut-associated lymphoid tissues (GALT). One of its primary responses to microbes is the secretion of IgA, whose role in the mucosa is vital for preventing pathogen colonization, invasion and spread. The mechanisms involved in these key responses include neutralization of pathogens, immune exclusion, immune modulation, and cross-protection. The generation and maintenance of high affinity IgA responses require a delicate balance of multiple components, including B and T cell interactions, innate cells, the cytokine milieu (e.g., IL-21, IL-10, TGF-β), and other factors essential for intestinal homeostasis, including the gut microbiota. In this review, we will discuss the main cellular components (e.g., T cells, innate lymphoid cells, dendritic cells) in the gut microenvironment as mediators of important effector responses and as critical players in supporting B cells in eliciting and maintaining IgA production, particularly in the context of enteric infections and vaccination in humans. Understanding the mechanisms of humoral and cellular components in protection could guide and accelerate the development of more effective mucosal vaccines and therapeutic interventions to efficiently combat mucosal infections.

    Keywords: IgA, Enteric diseases, T cells, long term immune response, vaccination and CHIM

    Received: 08 Jun 2024; Accepted: 26 Aug 2024.

    Copyright: © 2024 Carreto-Binaghi, Sztein and Booth. 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:
    Marcelo B. Sztein, Center for Vaccine Development, School of Medicine, University of Maryland, Baltimore, United States
    Jayaum S. Booth, Center for Vaccine Development, School of Medicine, University of Maryland, Baltimore, United States

    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.