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Recent Molecular Research in Colitis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 October 2026 | Viewed by 1632

Editors


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Guest Editor
Department of Physiology, University of Seville, 41009 Seville, Spain
Interests: aquaporins; neurological biomarkers; NMO; blood–brain barrier; gut–brain axis
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Facultad de Farmacia, University of Seville, Seville, Spain
Interests: colitis; colon cancer; neuroinflammation; Alzheimer's disease

Special Issue Information

Dear Colleagues,

Colitis, a form of inflammatory bowel disease (IBD), is a chronic condition causing intestinal inflammation and significant health burdens. Symptoms include diarrhea, abdominal pain, and systemic complications, severely affecting patients' quality of life. Despite ongoing research, key molecular mechanisms remain unclear, highlighting the need for further investigation. The gut-brain axis plays a crucial role in colitis pathophysiology, linking intestinal inflammation with neurological and psychological symptoms such as anxiety, depression, and cognitive dysfunction. Factors like dysbiosis, increased intestinal permeability, and immune dysregulation contribute to both gastrointestinal and extraintestinal manifestations. Understanding these interactions could lead to novel therapeutic strategies targeting not only intestinal inflammation but also systemic effects. Advancing knowledge in this area is essential for improving treatment outcomes and patient well-being.

Prof. Dr. Pablo García-Miranda
Prof. Dr. María Vázquez-Carretero
Guest Editors

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Keywords

  • colitis
  • inflammatory bowel disease (IBD)
  • gut-brain axis
  • intestinal barrier
  • molecular mechanisms

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Published Papers (1 paper)

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Research

25 pages, 4663 KB  
Article
Characteristics of T-Cells Expressing IL-37 and Its Receptors in Inflammatory Bowel Disease
by Indiana Zorkau, Peter J. Eggenhuizen, Marie Lee, Steven X. Cho, Kylie R. James, Andrew M. Ellisdon, James C. Whisstock, Joshua D. Ooi, Marcel F. Nold, Claudia A. Nold-Petry and Rimma Goldberg
Int. J. Mol. Sci. 2026, 27(3), 1540; https://doi.org/10.3390/ijms27031540 - 4 Feb 2026
Cited by 3 | Viewed by 1094
Abstract
IBD pathogenesis is underpinned by an imbalance between excess inflammation caused by effector T-cells and inadequate suppression by regulatory T-cells (Tregs). Interleukin-37 (IL-37) is a potent, anti-inflammatory cytokine that signals via its receptors IL-1R5 and IL-1R8. Hence, augmenting anti-inflammatory mechanisms that drive IL-37 [...] Read more.
IBD pathogenesis is underpinned by an imbalance between excess inflammation caused by effector T-cells and inadequate suppression by regulatory T-cells (Tregs). Interleukin-37 (IL-37) is a potent, anti-inflammatory cytokine that signals via its receptors IL-1R5 and IL-1R8. Hence, augmenting anti-inflammatory mechanisms that drive IL-37 expression is a strategy to control IBD-associated inflammation. However, the role of IL-37 and its receptors in T-cells remains incompletely understood. Here, we investigated T-cell expression profiles of IL-37 and its receptors to understand the drivers of dysregulated T-cell responses in IBD and develop novel, more effective therapies. T-cell subsets from healthy control (HC), Crohn’s disease (CD) and ulcerative colitis (UC) peripheral blood mononuclear cells (PBMC) and lamina propria mononuclear cells (LPMC) were assessed for expression of IL-37 and its receptors by flow cytometry. CD3+IL-1R8+ T-cell transcriptomes underwent RNA sequencing. The phenotype and suppressive capacity of Tregs supplemented with IL-37 was assessed in vitro. Our results indicate that IL-37 and its receptors were differentially expressed among PBMC and LPMC T-cell subsets in IBD patients compared to HC. Transcription signatures unique to IBD were revealed, particularly histone and mitochondrial pathways. Remarkably, culturing Tregs with IL-37 preserved FOXP3 expression and suppressiveness at a level comparable to treatment with the well-established Treg stabilizing agent rapamycin. Altogether, our study identified differences in T-cells expressing IL-37 and its receptors that are indicative of T-cell dysfunction in IBD. These findings highlight a novel and promising avenue for restoring immune homeostasis in IBD by targeting and boosting the IL-37 signalling pathway. Full article
(This article belongs to the Special Issue Recent Molecular Research in Colitis)
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