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SummaryLong intergenic noncoding RNAs (lincRNAs) regulate biological processes in health and disease. Recent findings highlight the importance of lincRNAs in regulating T cell development and function. Here, we identified a lincRNA, LINC01871, which is highly induced upon CD4+ T cell activation and is predominantly located in the cytoplasm. The anti-inflammatory cytokine TGF-¦Â was found to suppress its expression. Silencing LINC01871 led to a modest decrease in IL-2 secretion. Notably, LINC01871 expression was highly specific to NK cells and T cells in several cross-tissue single cell RNA-seq atlases. These data suggest that LINC01871 is specifically expressed in T and NK cells and may contribute to T cell-mediated immunity in humans. Graphical abstract Highlights?LINC01871 is a cytoplasmic lincRNA induced upon CD4+ T cell activation?TGF-¦Â negatively regulates LINC01871 expression?Expression of LINC01871 is restricted to effector and memory T and NK cells Immunology; Molecular biology; Cell biology

Mare endometrosis is a chronic degenerative condition of the endometrium, primarily characterized by fibrosis, involving interactions among fibroblasts, immune cells, and epithelial cells regulated by cytokines and growth factors. T helper (Th)1 and Th2 cells seem to play a pivotal role in fibrosis. However, their roles in equine endometrial fibrosis remain unknown. This study explores Th1 and Th2 cell distribution across different stages of endometrium histopathological Kenney and Doig categories; and evaluated their secretome effects on non-fibrotic endometrium derived fibroblast functional characteristics, extracellular matrix (ECM)-associated mRNA transcription, and transcriptomic profiles. Th1 and Th2 cells, along with cytokines (IFN-¦Ã, IL-4, IL-13) and their receptors, were present in mare endometria at all endometrium stages. Th1 secretome influenced genes enriched in metabolism, cell cycle, and ECM-related pathways, while Th2 secretome regulated genes enriched in tissue remodeling and signaling pathways, suggesting their role in the development of fibrosis in the endometrosis progression.Supplementary InformationThe online version contains supplementary material available at 10.1038/s41598-025-20152-0.

Cytokines are key soluble signaling molecules that regulate immune responses. With the advent of therapies that selectively target cytokines and cytokine receptors, understanding the molecular mechanisms underpinning how immune cells integrate multiple cytokine signals has become a critical challenge in immunology. However, the pleiotropic nature of cytokines makes it difficult to decipher their precise contributions in various contexts. Here, we used an integrated experimental and computational approach to investigate the combined effect and interplay between the pro-inflammatory cytokine interleukin-6 (IL-6) and interferon-beta (IFN¦Â), also a pro-inflammatory cytokine with potent antiviral properties, in modulating regulatory T cell (Treg) induction. Our studies reveal that, in contrast with its pro-inflammatory role in innate immune responses, IFN¦Â can counteract the well-described inhibitory effect of IL-6 on Treg induction. Mechanistically, we demonstrate that IFN¦Â and IL-6 signal independently to promote opposing effects on the acetylation of Foxp3, an essential transcription factor governing Treg differentiation, stability, and function. We further show that this mechanism is conserved in both murine and human T cells, highlighting the broad relevance of this finding in immune regulation. These results have important implications for the numerous contexts in which IFN¦Â and IL-6 co-exist, including viral infection, transplantation, and autoimmune disease.