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NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE239704 | GEO | 2024/03/28

REPOSITORIES: GEO

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NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [sc_rna]

Project description:The outcome of cancer and autoimmunity is dictated by the recruitment and effector functions of CD4+ conventional T cells (Tconv cells). The NF-kappaB (NF-κB) family of transcription factors is implicated in different aspects of Tconv cell biology, but the cell-autonomous roles of NF-κB subunits are elusive. Here, we explored the contributions of canonical RelA and c-Rel subunits to Tconv function in health and disease. We found that RelA, rather than c-Rel, shaped the transcriptome of mouse and human Tconv cells at steady-state and was required for Tconv polarization toward the TH17 lineage in vitro. RelA-deficient mice were fully protected against neuro-inflammation in a mouse model of multiple sclerosis (MS), because of defective transition to a pathogenic TH17 gene expression program. In contrast, Tconv-restricted ablation of c-Rel, but not RelA, impaired their function in the microenvironment of transplanted tumors, resulting in enhanced cancer burden. c-Rel in Tconv cells was required for the response to PD-1-blockade therapy, and a c-Rel-dependent gene signature was correlated with better response and prognosis in anti-PD-1-treated patients. Our data demonstrate a division of labor between different subunits of the NF-κB pathway, paving the way for subunit-targeted immunotherapies.

2024-03-28 | GSE239703 | GEO

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_mouse]

2024-03-28 | GSE239700 | GEO

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_human]

2024-03-28 | GSE239698 | GEO

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer

Project description:NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer

| PRJNA1000587 | ENA

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [sc_rna]

Project description:NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [sc_rna]

| PRJNA1000594 | ENA

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_human]

Project description:NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_human]

| PRJNA1000589 | ENA

NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_mouse]

Project description:NF-κB transcription factors RelA and c-Rel selectively control CD4+ T-cell function in multiple sclerosis and cancer [bulk_mouse]

| PRJNA1000591 | ENA

Differential requirements for the canonical NF-κB transcription factors c-REL and RELA during the generation and activation of mature B cells.

Project description:Signaling through the canonical nuclear factor-κB (NF-κB) pathway is critical for the generation and maintenance of mature B cells and for antigen-dependent B-cell activation. c-REL (rel) and RELA (rela) are the downstream transcriptional activators of the canonical NF-κB pathway. Studies of B cells derived from constitutional rel knockout mice and chimeric mice repopulated with rela-/- fetal liver cells provided evidence that the subunits can have distinct roles during B-cell development. However, the B cell-intrinsic functions of c-REL and RELA during B-cell generation and antigen-dependent B-cell activation have not been determined in vivo. To clarify this issue, we crossed mice with conditional rel and rela alleles individually or in combination to mice that express Cre-recombinase in B cells. We here report that, whereas single deletion of rel or rela did not impair mature B-cell generation and maintenance, their simultaneous deletion led to a dramatic reduction of follicular and marginal zone B cells. Upon T cell-dependent immunization, B cell-specific deletion of the c-REL subunit alone abrogated the formation of germinal centers (GCs), whereas rela deletion did not affect GC formation. T-independent responses were strongly impaired in mice with B cell-specific deletion of rel, and only modestly in mice with RELA-deficient B cells. Our findings identify differential requirements for the canonical NF-κB subunits c-REL and RELA at distinct stages of mature B-cell development. The subunits are jointly required for the generation of mature B cells. During antigen-dependent B-cell activation, c-REL is the critical subunit required for the initiation of the GC reaction and for optimal T-independent antibody responses, with RELA being largely dispensable at this stage.

| S-EPMC5360551 | biostudies-literature

Rel/NF-κB Transcription Factors Emerged at the Onset of Opisthokonts.

Project description:The Rel/NF-κB transcription factor family has myriad roles in immunity, development, and differentiation in animals, and was considered a key innovation for animal multicellularity. Rel homology domain-containing proteins were previously hypothesized to have originated in a last common ancestor of animals and some of their closest unicellular relatives. However, key taxa were missing from previous analyses, necessitating a systematic investigation into the distribution and evolution of these proteins. Here, we address this knowledge gap by surveying taxonomically broad data from eukaryotes, with a special emphasis on lineages closely related to animals. We report an earlier origin for Rel/NF-κB proteins than previously described, in the last common ancestor of animals and fungi, and show that even in the sister group to fungi, these proteins contain elements that in animals are necessary for the subcellular regulation of Rel/NF-κB.

| S-EPMC8763368 | biostudies-literature

Nuclear Factor κB (NF-κB)-Mediated Inflammation in Multiple Sclerosis.

Project description:The nuclear factor κB (NF-κB) signaling cascade has been implicating in a broad range of biological processes, including inflammation, cell proliferation, differentiation, and apoptosis. The past three decades have witnessed a great progress in understanding the impact of aberrant NF-κB regulation on human autoimmune and inflammatory disorders. In this review, we discuss how aberrant NF-κB activation contributes to multiple sclerosis, a typical inflammatory demyelinating disease of the central nervous system, and its involvement in developing potential therapeutic targets.

| S-EPMC7105607 | biostudies-literature

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