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IL-6-induced C/EBPα drives follicular regulatory T cell differentiation to regulate humoral immunity in mice

ABSTRACT: To investigate the C/EBPα-dependent mechanism of follicular regulatory T (Tfr) cell differentiation and function under pathological settings, we analyzed the transcriptomic profile of wild-type (WT) and Cebpa knock-out (KO) Tfr cells in autoimmune condition.

ORGANISM(S): Mus musculus

PROVIDER: GSE289950 | GEO | 2026/05/31

REPOSITORIES: GEO

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IL-6-induced C/EBPα drives follicular regulatory T cell differentiation to regulate humoral immunity in mice

Project description:Follicular regulatory T (Tfr) cells suppress Tfh-mediated B cell responses to regulate humoral immunity, yet the signaling pathway governing their differentiation remain largely undefined. In this study, we reveal that IL-6-induced C/EBPa is essential for Tfr cell differentiation and function in mice. To investigate whether C/EBPa directly regulates Tfr-related genes and identify endogenous C/EBPa binding targets in Tfr cells, we performed Cleavage Under Targets and Release Using Nuclease (CUT&RUN) sequencing in Tfr and CXCR5- Treg cells. Collectively, we identify the IL-6-C/EBPa-Bcl6/Cxcr5 axis as a central mechanism to promote Treg-to-Tfr differentiation to control pathogenic humoral immune responses.

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Store-operated Ca2+ entry in follicular T cells controls humoral immune responses and autoimmunity

Project description:T follicular helper (TFH) cells promote affinity maturation of B cells in germinal centers (GCs), whereas T follicular regulatory (TFR) cells limit GC reaction. Store-operated Ca2+ entry (SOCE) through Ca2+ release-activated Ca2+ (CRAC) channels mediated by STIM and ORAI proteins is a fundamental signaling pathway in T lymphocytes. Here we show that SOCE is required for the differentiation and function of both TFH and TFR cells. Conditional deletion of Stim1 and Stim2 genes in T cells or Treg cells results in spontaneous autoantibody production and humoral autoimmunity. Conversely, antibody-mediated immune responses following viral infection critically depend on SOCE in TFH cells. Mechanistically, STIM1 and STIM2 control early TFR and TFH cell differentiation through NFAT-mediated IRF4, BATF and Bcl-6 expression. SOCE plays a dual role in GC response by controlling TFH and TFR cell function, thus enabling protective B cell responses and preventing humoral autoimmunity. RNAseq analyses of WT and Stim1Stim2 DKO follicular T cells and non-follicular T cells; 4-6 mice per cohort in duplicates. Mice were infected for 10 days with LCMV.

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Store-operated Ca2+ entry in follicular T cells controls humoral immune responses and autoimmunity

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IL-12 drives the diferentiation of human T follicular regulatory cells [RNA-seq]

Project description:T follicular regulatory (Tfr) cells can counteract the B cell-helper activity of T follicular helper (Tfh) cells and hinder the production of antibodies against self-antigens or allergens. A mechanistic understanding of the cues initiating the differentiation of T regulatory (Treg) cells into Tfr cells, which is instrumental for the therapeutic manipulation of diseases associated with a Tfr cell imbalance, is still missing. Despite their opposed roles, Tfr and Tfh cell differentiation appears to be controlled by partially overlapping signals, including TCR stimulation and costimulatory molecules. However, it is still unknown if cytokines that have been shown to control the biology of human Tfh cells, including IL-12 and activin A, can influence the differentiation of Tfr cells. To address this question, we evaluated the impact of these two cytokines on the in vitro differentiation of Tfr cells. Herein, we report a role for IL-12 and down stream Stat4 chromatin binding in driving, on activated Treg cells, the induction of molecules that belong to the Tfr cell program, including CXCR5, PD-1, BCL6 and ICOS meanwhile preserving Tfr regulatory function.

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Project description:T follicular regulatory (TFR) cells are found in the germinal center (GC) response and help shape the antibody (Ab) response. Whether TFR cells have a suppressive role, a helper role or both types of roles in the GC is unclear. Here, we addressed TFR cell function using 3 different strains of TFR cell mutant mice. After immunization, GC B cells but not T follicular helper (TFH) cell positively correlated with TFR cell levels. Using a gene profiling approach, we found that TFH cells from TFR-deficient mice showed strong up-regulation of granzyme B (Gzmb) and other effector CD8 T cell genes, many of which were Stat4 dependent. This aberrant cytotoxic T cell gene profile was increased in TFR-deficient mice crossed on a pro-inflammatory background. We detected Gzmb+ and Eomesodermin+ TFH cells and a higher rate of apoptotic GC B cells in the absence of TFR cells. Klrg1+ TFH cells expressed higher Gzmb and less IL-4 and IL-21. Our data show that TFR cells repress the development of abnormal cytotoxic TFH cells that correlate with a lower GC and Ab response. This data shows a novel mode of helper function for TFR cells in the GC response.

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