ArticleClinical rheumatology2026
IL-33/ST2 induces Tfh cells activation and GCs formation in collagen-induced arthritis.
Article in Clinical rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe Interleukin-33 (IL-33) has a strong[AL1] pro-inflammatory effect on collagen-induce arthritis (CIA), a classic animal model of rheumatoid arthritis (RA). However, the underlying mechanism remains unclear. In this study, we investigated the presence of the IL-33 receptor suppression of tumorigenicity 2 (ST2) on T follicular helper (Tfh) cells and its impact on CIA through regulation of Tfh cells and germinal center (GC) B cells. [AL1]LE: Please check if the corresponding author's telecommunications data are correctly captured/indicated.
methodsIn vitro studies involved treating polarized Tfh cells with IL-33 to analyze its effects on Tfh differentiation by measuring ST2, PD-1, and CXCR5 expression using flow cytometry. C57BL/6J mice were immunized with keyhole limpet hemocyanin (KLH) and divided into three groups: control, KLH-only, and KLH+IL-33. Additionally, ST2
resultsIn vitro experiments showed that IL-33 promoted Tfh differentiation and survival. IL-33 disrupted the Tfr/Tfh balance in the KLH model. In CIA, IL-33 exacerbated arthritis severity by enhancing Tfh cell proliferation in LNs and significantly altering GC B cell development and antibody production.
conclusionThis study reveals a novel mechanism by which IL-33 exacerbates RA, suggesting its pro-inflammatory effects are mediated through Tfh cell polarization and GC activation. Key Points • The IL-33/ST2 axis promotes Tfh cell differentiation and viability. • IL-33 exacerbates arthropathy and enhances germinal center reactions in CIA mice. • IL-33 increases the Tfh cell ratio and ST2 expression on Tfh cells in CIA mice. • The IL-33/ST2 axis disrupts the Tfr/Tfh balance in KLH-immunized mice.
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