Hussain MS, Bisht AS, Gupta G. Reduced interleukin-2 receptor subunit γ expression in Crohn's disease: A potential mechanism for γδ T cell deficiency. World J Gastroenterol 2025; 31(13): 103180 [DOI: 10.3748/wjg.v31.i13.103180]
Corresponding Author of This Article
Md Sadique Hussain, PhD, Assistant Professor, Uttaranchal Institute of Pharmaceutical Sciences, Uttaranchal University, Prem Nagar, Dehra Dun 248007, Uttarākhand, India. sadiquehussain007@gmail.com
Research Domain of This Article
Immunology
Article-Type of This Article
Letter to the Editor
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Md Sadique Hussain, Uttaranchal Institute of Pharmaceutical Sciences, Uttaranchal University, Dehra Dun 248007, Uttarākhand, India
Ajay Singh Bisht, School of Pharmaceutical Sciences, Shri Guru Ram Rai University, Dehra Dun 248001, Uttarākhand, India
Gaurav Gupta, Centre for Research Impact & Outcome-Chitkara College of Pharmacy, Chitkara University, Rajpura 140401, Punjab, India
Gaurav Gupta, Centre of Medical and Bio-allied Health Sciences Research, Ajman University, Al Jerf 00000, Ajman, United Arab Emirates
Author contributions: Hussain MS contributed to conceptualization, data curation, writing - original draft; Bisht AS contributed to formal analysis, investigation, validation; Gupta G contributed to investigation, resources, supervision, writing - review & editing.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Md Sadique Hussain, PhD, Assistant Professor, Uttaranchal Institute of Pharmaceutical Sciences, Uttaranchal University, Prem Nagar, Dehra Dun 248007, Uttarākhand, India. sadiquehussain007@gmail.com
Received: November 12, 2024 Revised: January 26, 2025 Accepted: February 20, 2025 Published online: April 7, 2025 Processing time: 141 Days and 17.8 Hours
Abstract
Crohn’s disease (CD) is a chronic inflammatory disorder characterized by dysregulated immune responses and significant disruption of intestinal immunity. A recent case-control study by Andreu-Ballester et al revealed decreased expression of interleukin (IL)-2 receptor subunit γ (CD132) in CD tissues, a finding that has profound implications for understanding immune dysregulation in CD. CD132, an essential component of the IL-7/IL-2 signaling axis, is critical for γδ T cell survival and function, which are pivotal for maintaining gut integrity and modulating inflammation. Here, we propose that reduced CD132 expression represents a key mechanism underlying γδ T cell deficiencies in CD, contributing to impaired immune surveillance and exacerbated inflammation. This hypothesis integrates emerging evidence from cytokine signaling and immunopathology in CD, offering new insights into its pathogenesis. These findings highlight the therapeutic potential of targeting the IL-7/IL-2 axis to restore immune homeostasis in CD, presenting a novel avenue for future research and intervention.
Core Tip: Crohn’s disease (CD) is characterized by immune dysregulation, with reduced expression of the interleukin (IL)-2 receptor γ subunit (CD132) playing a pivotal role. CD132 is essential for IL-7/IL-2 signaling, which supports γδ T cell survival and function. Its downregulation impairs immune surveillance, exacerbates γδ T cell deficiency, and contributes to inflammation. This study highlights the therapeutic potential of targeting the IL-7/IL-2 axis to restore immune homeostasis in CD. Future research should explore CD132 modulation as a novel strategy to mitigate γδ T cell dysfunction and improve outcomes for CD patients.
