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RNA-Seq analysis of germinal center B cells from Tfr-depleted and control kidney transplant recipients

ABSTRACT: Assessment of transcriptional programs of germinal center B cells isolated from lymph nodes of Tfr-depleted (Tfr-DTR) and control (Tfr-Con) recipients post-transplantation to investigate the role of Tfr cells in kidney transplant rejection.

ORGANISM(S): Mus musculus

PROVIDER: GSE286974 | GEO | 2025/02/15

REPOSITORIES: GEO

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Tfr Cells Restrain Rejection of Kidney Allografts by Limiting Pro-Inflammatory Cytokines in B cells [scRNA-seq]

Project description:Pathogenic antibodies produced by alloreactive B cells mediate antibody-mediated rejection (ABMR) after kidney transplantation, but the mechanisms controlling these antibodies remain poorly understood. Follicular Regulatory T (Tfr) cells modulate follicular helper T (Tfh) cell-mediated B cell responses but their roles in controlling alloreactive antibody are unknown. Here, we studied the developmental signals and functions of Tfr cells in allogeneic kidney transplantation. We show that costimulatory blockade alters the development of Tfr cells disproportionately by decreasing germinal center (GC)-like Tfr cells and increasing follicular-like Tfr cells. Functionally, Tfr cell deletion resulted in accelerated rejection and increases in donor-specific B cells in both draining lymph nodes and kidney allografts. Mechanistically, Tfr cell deletion increased GC B cell expression of pro-inflammatory cytokines such as IL-15. Neutralization of IL-15 compensated for the loss of Tfr cells and prolonged kidney transplant recipient survival. Together these data demonstrate the signals for Tfr cell development and how these cells restrain rejection by limiting alloreactive B cell responses.

2025-02-15 | GSE286055 | GEO

Withdrawal of immunosuppressive therapy in stable liver transplant recipients

Project description:Complications due to long-term administration of immunosuppressive therapy increase the morbidity and mortality of liver transplant recipients. Discontinuation of immunosuppressive drugs in recipients spontaneously developing operational tolerance could substantially lessen this burden. However, this strategy results in the development of rejection in a high proportion of recipients who require lifelong immunosuppression. Thus, there is a need to identify predictive factors of successful drug withdrawal and to define the clinical and histological outcomes of operationally tolerant liver recipients. Methods. We enrolled 102 stable liver transplant recipients in an immunosuppression withdrawal trial in which drugs were gradually discontinued over a 6-9 month period. Patients with stable graft function and no signs of rejection in a liver biopsy conducted 12 months after cessation of immunosuppressive therapy were considered operationally tolerant. Results. Out of the 98 recipients who completed the study, immunosuppression discontinuation was successful in 41 recipients and rejection occurred in 57. Rejection episodes were mild and were resolved in all cases. Development of tolerance was independently associated with time elapsed since transplantation, recipient age, and male gender. No histological damage was apparent in protocol biopsies performed after successful drug withdrawal.

2012-01-09 | GSE28842 | GEO

Human T follicular helper cells seed the germinal center-resident regulatory pool

Project description:FOXP3+ T follicular regulatory cells (Tfrs) control germinal center (GC) responses by steering antibody formation away from self-reactivity and toward microbe/vaccine recognition. As originally described, murine Tfr cells descend exclusively from thymically-derived, self-antigen recognizing, T regulatory cells (Tregs), but newer animal models suggest vaccine-recognizing T follicular helper (Tfh) cells can assume regulatory roles as GCs mature. To test the hypothesis that the human Tfr pool is heterogenous in function and provenance, we used paired TCRVA and TCRVB sequencing to distinguish tonsillar Tfr cells clonally related to the natural Tregs (nTfr) from those induced from Tfh cells (iTfr). Through in silico predictions and in vitro tonsillar organoid lineage tracking, we identified a Tfh to iTfr developmental trajectory that passed through a distinct CD25hiBLIMP1+FOXP3- transitional stage. The genes and proteins that iTfr and nTfr cells express differentially were utilized as handles to precisely pinpoint the in situ locations of cells from each subset via multi-plex microscopy and to establish divergent functional adaptations. In total, we characterize human iTfr cells as a GC-resident CD38+ Tfr subset that descend from Tfh lineage cells to gain suppressive qualities while retaining their capacity for GC B-cell help.

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FoxP3 and Ezh2 Regulate Tfr cell Suppressive Function and Transcriptional Program [InVitro Ex-Tfr]

Project description:InVitro Ex-Tfr RNAseq

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Decreased TFR/TFH ratio in SIV-infected rhesus macaques may contribute to accumulation of TFH cells in chronic infection

Project description:T follicular helper cells (TFH) are critical for the development and maintenance of germinal centers (GC) and humoral immune responses. During chronic HIV/SIV infection TFH accumulate, possibly as a result of antigen persistence. The HIV/SIV-associated TFH expansion may also reflect lack of regulation by suppressive follicular regulatory CD4+ T-cells (TFR). TFR are natural regulatory T-cells (TREG) that migrate into the follicle and, similarly to TFH, up-regulate CXCR5, Bcl-6, and PD1. Here we identified TFR as CD4+CD25+FoxP3+CXCR5+PD1hiBcl-6+ within lymph nodes of rhesus macaques (RM) and confirmed their localization within the GC by immunohistochemistry. RNA sequencing showed that TFR exhibit a distinct transcriptional profile with shared features of both TFH and TREG, including intermediate expression of FoxP3, Bcl-6, PRDM1, IL-10, and IL-21. In healthy, SIV-uninfected RM, we observed a negative correlation between frequencies of TFR and both TFH and GC B-cells as well as levels of CD4+ T-cell proliferation. Following SIV infection, the TFR/TFH ratio was reduced with no change in the frequency of TREG or TFR within the total CD4+ T-cell pool. Finally, we examined whether higher levels of direct virus infection of TFR were responsible for their relative depletion post-SIV infection. We found that TFH, TFR and TREG sorted from SIV- infected RM harbor comparable levels of cell-associated viral DNA. Our data suggests that TFR may contribute to the regulation and proliferation of TFH and GC B-cells in vivo and that a decreased TFR/TFH ratio in chronic SIV infection may lead to unchecked expansion of both TFH and GC B-cells. TFR, TFH, TREG and bulk CD4 cells were sorted from spleens of 5 uninfected and 5 infected RM.

2015-09-02 | E-GEOD-69756 | biostudies-arrayexpress

Data regarding transplant induced germinal center humoral autoimmunity.

Project description:This data is related to the research article entitled "Germinal center humoral autoimmunity independently mediates progression of allograft vasculopathy" (Harper et al., 2016) [2]. The data presented here focuses on the humoral autoimmune response triggered by transferred allogeneic CD4 T cells and includes details on: (a) the recipient splenic germinal center (GC) response; (b) augmentation of humoral autoimmunity and accelerated heart allograft rejection following transplantation from donors primed against recipient; (c) flow cytometric analysis of donor and recipient CD4 T cells for signature markers of T follicular helper cell differentiation; (d) in vitro donor endothelial cell migration in response to column purified autoantibody from recipient sera; (e) analysis of development of humoral responses in recipients following adoptive transfer of donor CD4 T cells and; (f) the development of humoral autoimmunity in mixed haematopoietic chimeric mice.

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Transcriptomic profiling of blood memory B cell subsets in kidney transplant recipients

Project description:We compared the transcriptomic profile between patients without donor-specific antibodies (DSA-), patients with donor-specific antibodies without antibody-mediated rejection (DSA+ ABMR-) and patients with donor-specific antibodies and antibody-mediated rejection (DSA+ ABMR+). We found that patients with DSA+ ABMR+ had a distinct transcriptomic profile compared to DSA- and DSA+ ABMR- patients, characterized by upregulation of genes related to B cell activation and B cell effector functions.

2021-07-14 | GSE155670 | GEO

Transcriptomic profiling of circulating T follicular helper cells in kidney transplant recipients

Project description:We compared the transcriptomic profile between patients without donor-specific HLA antibodies (DSA-), patients with donor-specific HLA antibodies without antibody-mediated rejection (DSA+ ABMR-) and patients with donor-specific HLA antibodies and antibody-mediated rejection (DSA+ ABMR+). We found that patient with DSA+ ABMR+ had a distinct transcriptomic profile compared to DSA- and DSA+ ABMR-, characterized by upregulation of genes encoding for germinal center T follicular helper cells function, T-B cell interaction and costimulatory molecules.

2021-07-01 | GSE134477 | GEO

Regulation of TFR cells by Blimp1

Project description:What genes does the transcription factor Blimp1 regulate in Tfr cells?

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Gene expression profile at single cell level of FACS-sorted blood NK cells from kidney transplant recipients

Project description:We explored NK cell differential gene expression profiles in patients with antibody-mediated rejection versus T-cell mediated rejection.

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