Background: ZEB1, a zinc-finger E homeobox-binding transcription factor most frequently associated with developmental programs linked to epithelial-mesenchymal transition, has been demonstrated to regulate immune cell function. The study aimed to investigate the expression pattern of ZEB1 in Th17 cells and its colocalization with p-STAT3 in human apical periodontitis lesions.
Methods: Thirty-nine human periapical tissues were collected for ex vivo study, including periapical granulomas (PGs, n = 14), radicular cysts (RCs, n = 12), and healthy control tissues (control group, n = 13). Inflammatory infiltration of the lesions was assessed using hematoxylin-eosin staining. The expression of ZEB1 was detected and analyzed by immunohistochemistry. The localization of ZEB1 in Th17 cells and its colocalization with p-STAT3 were assessed using fluorescence colocalization.
Results: ZEB1 expression was significantly higher in PGs and RCs than in the healthy control group; however no significant difference between the two groups was observed. Immunofluorescence analysis revealed that ZEB1 expression was correlated with IL17 and CD4 double-positive cells in human periapical lesions. ZEB1/ p-STAT3 double-positive cells were predominant in RCs and PGs than in the healthy control group.
Conclusions: The expression of ZEB1 was significantly elevated in PGs and RCs, and correlated with Th17 cells and p-STAT3 expression. This study revealed that ZEB1 is a potential player correlated with STAT3 activation and Th17 cells in apical periodontitis pathogenesis.
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http://dx.doi.org/10.1186/s12903-025-05633-y | DOI Listing |
Gut
March 2025
Department of Gastroenterology, Shanghai Tenth People's Hospital, Shanghai, China
Background: GPR171 suppresses T cell immune responses involved in antitumour immunity, while its role in inflammatory bowel disease (IBD) pathogenesis remains unclear.
Objective: We aimed to investigate the role of GPR171 in modulating CD4 T cell effector functions in IBD and evaluate its therapeutic potential.
Design: We analysed GPR171 expression in colon biopsies and peripheral blood samples from patients with IBD and assessed the impact of GPR171 on CD4 T cell differentiation through administration of its endogenous ligand (BigLEN).
J Immunol
February 2025
La Jolla Institute for Immunology, La Jolla, CA, United States.
A fundamental dichotomy in lymphocytes separates adaptive T and B lymphocytes, with clonally expressed antigen receptors, from innate lymphocytes, which carry out more rapid responses. Some T cell populations, however, are intermediates between these 2 poles, with the capacity to respond rapidly through T cell receptor activation or by cytokine stimulation. Here, using publicly available datasets, we constructed linear mixed models that not only define a gradient of innate gene expression in common for mouse innate-like T cells, but also are applicable to other mouse T lymphoid populations.
View Article and Find Full Text PDFLiver fibrosis is a global health problem. IL-17A has proven profibrogenic properties in liver disease making it an interesting therapeutic target. IL-17A is regulated by RORγt and produced by Th17 CD4+ and γδ-T cells.
View Article and Find Full Text PDFJ Immunol
February 2025
Genentech, Inc, South San Francisco, CA, United States.
A gene encoding the transcription factor RTF1 has been associated with an increased risk of ulcerative colitis (UC). In this study, we investigated its function in modulating T cells expressing interleukin-17A (Th17 cells), a cardinal cell type promoting intestinal inflammation. Our results indicate that Rtf1 deficiency disrupts the differentiation of Th17 cells, while leaving regulatory T cells (Treg) unaffected.
View Article and Find Full Text PDFClin Rev Allergy Immunol
March 2025
School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Uveitis involves a complex interplay of immune cell infiltration and cytokine imbalances, with Th17 cells playing a central role in this process. Th17 cells contribute to disease pathogenesis by promoting inflammation, recruiting additional immune cells, and directly damaging retinal tissues. This review discusses the current knowledge on therapeutic strategies targeting Th17-related cytokines, including cytokine blockade, small molecule inhibitors, and immunomodulatory approaches.
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