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Role of Gut Microbiota in Immune Tolerance and Vaccine Development

A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: 31 December 2024 | Viewed by 811

Special Issue Editor


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Guest Editor
Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang, Republic of Korea
Interests: gut microbiota; immune regulation; microbiome therapeutics; immune tolerance; autoimmunity; allergy; cancer
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Special Issue Information

Dear Colleagues,

Immune tolerance, also known as immunological tolerance, refers to a state of active and highly regulated unresponsiveness of the immune system to self-antigens or a specific antigen that can induce an immune response in the body. It plays a crucial role in normal physiology, and deficiencies in tolerance can lead to autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, and type 1 diabetes.

In recent years, considerable progress has been made in immune tolerance research, particularly in the fields of immunotherapy, immunomodulation, and immune system regulation. However, challenges persist due to incomplete knowledge of the exact mechanisms, a lack of suitable research models, and limited access to clinical data, making it difficult to develop effective treatments for diverse immune tolerance-related disorders.

This Special Issue will specifically address (but is not limited to) the following two topics:

  1. Cellular Aspects of Immune Tolerance in Health and Diseases: The Role of Immune Cell Subtypes and Their Crosstalk.

Immune tolerance involves interactions among various immune cell subtypes, such as T cells, B cells, macrophages, and dendritic cells. Crosstalk between these immune cell subtypes regulates the development of immune tolerance, enabling the body to recognize and accept self-antigens without triggering an immune response.

  1. The Role of Commensal Microbiota in Immune Tolerance and Vaccines.

Microorganisms, including beneficial bacteria in and on the body, play a vital role. Diseases like inflammatory bowel disease, allergies, asthma, and diabetes are linked to changes in microbiome composition. Commensal bacteria can reduce inflammation, downregulate pro-inflammatory responses, and enhance vaccine efficacy. Furthermore, they stimulate the production of protective antibodies, increasing vaccine effectiveness.

We welcome all types of articles, including original research, comprehensive and systematic reviews, brief reports, etc., for this Special Issue. We eagerly anticipate receiving your contributions.

Prof. Dr. Sin-Hyeog Im
Guest Editor

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Keywords

  • immune tolerance
  • subtype of immune cells
  • microbiome
  • probiotics
  • T cells
  • B cells
  • dendritic cells
  • antigen-presenting cells

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Published Papers (1 paper)

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Research

13 pages, 4452 KiB  
Article
IL-33 Induces a Switch in Intestinal Metabolites Revealing the Tryptophan Pathway as a Target for Inducing Allograft Survival
by Camila Pinto, Tomás Carrasco-Loncharic, Eduardo González-Mienert, Javiera de Solminihac, Felipe Gálvez-Jirón, Federico Cifuentes and Karina Pino-Lagos
Nutrients 2024, 16(21), 3655; https://doi.org/10.3390/nu16213655 - 27 Oct 2024
Viewed by 665
Abstract
Background: IL-33, a pleiotropic cytokine, has been associated with a plethora of immune-related processes, both inflammatory and anti-inflammatory. T regulatory (Treg) cells, the main leukocyte population involved in immune tolerance, can be induced by the administration of IL-33, the local microbiota, and its [...] Read more.
Background: IL-33, a pleiotropic cytokine, has been associated with a plethora of immune-related processes, both inflammatory and anti-inflammatory. T regulatory (Treg) cells, the main leukocyte population involved in immune tolerance, can be induced by the administration of IL-33, the local microbiota, and its metabolites. Here, we demonstrate that IL-33 drastically induces the production of intestinal metabolites involved on tryptophan (Trp) metabolism. Methods: naïve mice were treated with IL-33 for 4 days and leukocyte populations were analyzed by flow cytometry, and feces were processed for microbiota and intestinal metabolites studies. Using a murine skin transplantation model, the effect of Kynurenic acid (KA) on allograft survival was tested. Results: Under homeostatic conditions, animals treated with IL-33 showed an increment in Treg cell frequencies. Intestinal bacterial abundance analysis indicates that IL-33 provokes dysbiosis, demonstrated by a reduction in Enterobacteria and an increment in Lactobacillus genera. Furthermore, metabolomics analysis showed a dramatic IL-33 effect on the abundance of intestinal metabolites related to amino acid synthesis pathways, highlighting molecules linked to Trp metabolism, such as kynurenic acid (KA), 5-Hydroxyindoleacetic acid (5-HIAA), and 6-Hydroxynicotinic acid (6-HNA), which was supported by an enhanced expression of Ido and Kat mRNA in MLN cells, which are two enzymes involved on KA synthesis. Interestingly, animals receiving KA in drinking water and subjected to skin transplantation showed allograft acceptance, which is associated with an increment in Treg cell frequencies. Conclusions: Our study reveals a new property for IL-33 as a modulator of the intestinal microbiota and metabolites, especially those involved with Trp metabolism. In addition, we demonstrate that KA favors Tregs in vivo, positively affecting skin transplantation survival. Full article
(This article belongs to the Special Issue Role of Gut Microbiota in Immune Tolerance and Vaccine Development)
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