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Single cell transcriptome and surface protein expression analysis identify OX40+GITR+ pathogenic T helper 17 in anklyosing spondilytis.

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE216885 | GEO | 2023/02/23

REPOSITORIES: GEO

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Single cell transcriptome and surface protein expression analysis identify OX40+GITR+ pathogenic T helper 17 in anklyosing spondilytis [CITE-seq]

Project description:We unveiled the characteristics of pTh17s, which are polyfunctional IL-17A and IFN-γ-producing memory CD4+ T cells. scRNA-seq and cytometry analysis found that the co-expression of OX40 and GITR is increased in pTh17 cells.

2023-02-23 | GSE216884 | GEO

Single cell transcriptome and surface protein expression analysis identify OX40+GITR+ pathogenic T helper 17 in anklyosing spondilytis [scRNA-seq]

2023-02-23 | GSE216883 | GEO

Single cell transcriptome and surface protein expression analysis identify OX40+GITR+ pathogenic T helper 17 in anklyosing spondilytis.

Project description:Single cell transcriptome and surface protein expression analysis identify OX40+GITR+ pathogenic T helper 17 in anklyosing spondilytis.

| PRJNA896106 | ENA

Single cell transcriptome and surface protein expression analysis identify OX40+GITR+ pathogenic T helper 17 in anklyosing spondilytis [CITE-seq]

Project description:Single cell transcriptome and surface protein expression analysis identify OX40+GITR+ pathogenic T helper 17 in anklyosing spondilytis [CITE-seq]

| PRJNA896110 | ENA

Single cell transcriptome and surface protein expression analysis identify OX40+GITR+ pathogenic T helper 17 in anklyosing spondilytis [scRNA-seq]

Project description:Single cell transcriptome and surface protein expression analysis identify OX40+GITR+ pathogenic T helper 17 in anklyosing spondilytis [scRNA-seq]

| PRJNA896111 | ENA

T-Cell-Intrinsic Receptor Interacting Protein 2 Regulates Pathogenic T Helper 17 Cell Differentiation.

Project description:Receptor interacting protein 2 (RIP2) plays a role in sensing intracellular pathogens, but its function in T cells is unclear. We show that RIP2 deficiency in CD4+ T cells resulted in chronic and severe interleukin-17A-mediated inflammation during Chlamydia pneumoniae lung infection, increased T helper 17 (Th17) cell formation in lungs of infected mice, accelerated atherosclerosis, and more severe experimental autoimmune encephalomyelitis. While RIP2 deficiency resulted in reduced conventional Th17 cell differentiation, it led to significantly enhanced differentiation of pathogenic (p)Th17 cells, which was dependent on ROR? transcription factor and interleukin-1 but independent of nucleotide oligomerization domain (NOD) 1 and 2. Overexpression of RIP2 resulted in suppression of pTh17 cell differentiation, an effect mediated by its CARD domain, and phenocopied by a cell-permeable RIP2 CARD peptide. Our data suggest that RIP2 has a T cell-intrinsic role in determining the balance between homeostatic and pathogenic Th17 cell responses.

| S-EPMC6260980 | biostudies-literature

Analysis of GITR and OX40 signaling complexes

Project description:T cells are pivotal in the adaptive immune defense, necessitating a delicate balance between robust response against infections and self-tolerance. Their activation involves intricate cross-talk among signaling pathways triggered by the T-cell antigen receptors (TCR) and co-stimulatory or inhibitory receptors. The molecular regulation of these complex signaling networks is still incompletely understood. We identified an adaptor protein, ABIN1 as a component of the signaling complexes of GITR and OX40 co-stimulation receptors. T cells lacking ABIN1 exhibit hyper-responsiveness to TCR activation ex vivo, enhanced responses to cognate infections, and superior ability to induce experimental autoimmune diabetes in mice. We observed that ABIN1 negatively regulates NFκB and p38 pathways. The latter was at least partially responsible for the upregulation of key effector proteins, IFNG and GZMB in ABIN1-deficient T cells after TCR stimulation. Our findings reveal the intricate role of ABIN1 in T-cell regulation and its potential as a target for therapeutic fine-tuning T-cell responses.

2024-04-25 | PXD046422 | Pride

RAS P21 Protein Activator 3 (RASA3) Specifically Promotes Pathogenic T Helper 17 Cell Generation by Repressing T-Helper-2-Cell-Biased Programs.

Project description:Pathogenic Th17 (pTh17) cells drive inflammation and immune-pathology, but whether pTh17 cells are a Th17 cell subset whose generation is under specific molecular control remains unaddressed. We found that Ras p21 protein activator 3 (RASA3) was highly expressed by pTh17 cells relative to non-pTh17 cells and was required specifically for pTh17 generation in vitro and in vivo. Mice conditionally deficient for Rasa3 in T cells showed less pathology during experimental autoimmune encephalomyelitis. Rasa3-deficient T cells acquired a Th2 cell-biased program that dominantly trans-suppressed pTh17 cell generation via interleukin 4 production. The Th2 cell bias of Rasa3-deficient T cells was due to aberrantly elevated transcription factor IRF4 expression. RASA3 promoted proteasome-mediated IRF4 protein degradation by facilitating interaction of IRF4 with E3-ubiquitin ligase Cbl-b. Therefore, a RASA3-IRF4-Cbl-b pathway specifically directs pTh17 cell generation by balancing reciprocal Th17-Th2 cell programs. These findings indicate that a distinct molecular program directs pTh17 cell generation and reveals targets for treating pTh17 cell-related pathology and diseases.

| S-EPMC6249088 | biostudies-literature

T helper 17 cells play a critical pathogenic role in lung cancer.

Project description:Lung cancer development is associated with extensive pulmonary inflammation. In addition, the linkage between chronic obstructive pulmonary disease (COPD) and lung cancer has been demonstrated in population-based studies. IL-17-producing CD4 helper T cells (Th17 cells) play a critical role in promoting chronic tissue inflammation. Although Th17 cells are found in human COPD and lung cancer, their role is not understood. We have thus used a mouse model of lung cancer, in which an oncogenic form of K-ras (K-ras(G12D)), frequently found in human lung cancer, is restrictedly expressed in lung epithelial cells [via Clara cell secretory protein (CCSP(cre))]. In this model, Th17 and Treg but not Th1 cells were found enriched at the tumor tissues. When CCSP(cre)/K-ras(G12D) mice were weekly challenged with a lysate of nontypeable Haemophilus influenza (NTHi), which induces COPD-type inflammation and accelerates the tumor growth, they showed greatly enhanced Th17 cell infiltration in the lung tissues. Lack of IL-17, but not IL-17F, resulted in a significant reduction in lung tumor numbers in CCSP(cre)/K-ras(G12D) mice and also those treated with NTHi. Absence of IL-17 not only resulted in reduction of tumor cell proliferation and angiogenesis, but also decreased the expression of proinflammatory mediators and reduced recruitment of myeloid cells. Depletion of Gr-1(+)CD11b(+) myeloid cells in CCSP(cre)/K-ras(G12D) mice suppressed tumor growth in lung, indicating Gr-1(+)CD11b(+) myeloid cells recruited by IL-17 play a protumor role. Taken together, our data demonstrate a critical role for Th17 cell-mediated inflammation in lung tumorigenesis and suggest a novel way for prevention and treatment of this disease.

| S-EPMC3992670 | biostudies-literature

Surface-bound bovine serum albumin carrier protein as present in recombinant cytokine preparations amplifies T helper 17 cell polarization.

Project description:Understanding of T helper 17 lineage (TH17) polarization has been significantly promoted by cell culture experiments that reduce the complexity of the in vivo environment. We here investigated TH17 amplification by coating of cytokine preparations. Cytokine preparations coated to the surface compared to the same amount given in solution significantly enhanced TH17 polarization assessed by flow cytometry and interleukin (IL)-17A, IL-17F and RORγt mRNA expression. T cell proliferation and TH1 polarization were similarly enhanced while TREG polarization was impeded. TH17 amplification was replicated by coating the plate with low amounts of FCS or albumin as used as carrier protein for cytokines (0.5 μl 0.1%). It was unaltered by filtration, protein digestion and arylhydrocarbon receptor blockade, not replicated by LPS and independent of integrin stimulation. TH17 amplification required anti-CD3 stimulation and was T cell intrinsic. Supernatants of CD4+ cells polarized on coated cytokine preparations with carrier albumin conferred amplification to fresh splenocytes. Coating markedly elevated CD4+ IL-22 mRNA expression and IL-22 blockade significantly reduced TH17 amplification. Our data show TH17 amplification by coated albumin in the low amounts present in recombinant cytokine preparations. This unexpected adjuvant like effect underscores the need for controls also for temporal and spatial factors in cell culture.

| S-EPMC5093436 | biostudies-literature

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