Skip to main content

MINI REVIEW article

Front. Cell Dev. Biol.
Sec. Signaling
Volume 12 - 2024 | doi: 10.3389/fcell.2024.1429736
This article is part of the Research Topic Immunoregulation by Adenosine Signaling in Infection and Inflammation View all articles

ADENOSINE-MEDIATED IMMUNE RESPONSES IN INFLAMMATORY BOWEL DISEASE

Provisionally accepted
  • 1 Novartis Institutes for BioMedical Research, Basel, Switzerland
  • 2 University of Ferrara, Ferrara, Emilia-Romagna, Italy
  • 3 Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States

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

    Extracellular ATP and its derivates mediate a signaling pathway that might be pharmacologically targeted to treat inflammatory conditions. Extracellular adenosine, the product of ATP hydrolysis by ectonucleotidase enzymes, plays a key role in halting inflammation while promoting immune tolerance. The rate-limiting ectoenzyme ENTPD1/CD39 and the ecto-5′-nucleotidase/CD73 are the prototype members of the ectonucleotidase family, being responsible for ATP degradation into immunosuppressive adenosine. The biological effects of adenosine are mediated via adenosine receptors, a family of G protein-coupled receptors largely expressed on immune cells where they modulate innate and adaptive immune responses.Inflammatory bowel disease (IBD) is a serious inflammatory condition of the gastrointestinal tract, associated with substantial morbidity and often refractory to currently available medications. IBD is linked to altered interactions between the gut microbiota and the immune system in genetically predisposed individuals. A wealth of studies conducted in patients and animal models highlighted the role of various adenosine receptors in the modulation of chronic inflammatory diseases like IBD.In this review, we will discuss the most recent findings on adenosine-mediated immune responses in different cell types, with a focus on IBD and its most common manifestations, Crohn's disease and ulcerative colitis.

    Keywords: Adenosine, inflammatory bowel disease, Inflammation, ATP, adenosine receptors

    Received: 08 May 2024; Accepted: 16 Jul 2024.

    Copyright: © 2024 Vuerich, Ferrari and Longhi. 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:
    Davide Ferrari, University of Ferrara, Ferrara, 44121, Emilia-Romagna, Italy
    Maria Serena Longhi, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, Massachusetts, 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.