Comparision of expression profile between CD4+ helper T cells and CD8+ cytotoxic T cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE67204 | GEO | 2015/06/30
SECONDARY ACCESSION(S): PRJNA279262
REPOSITORIES: GEO
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Project description:We compared gene expression profiling between CD4+ helper T cells and CD8+ cytotoxic T cells CD4+ helper T cells vs CD8+ cytotoxic T cells
2015-06-30 | E-GEOD-67204 | biostudies-arrayexpress
Project description:CD4+ memory T helper cells are organized in different subsets characterized by distinct functions and chemokine receptor expression patterns induced and maintained by divergent gene programs. We demonstrate here that identical chemokine receptor combinations are sufficient to separate analogous differentiated CD8+ memory T cell subsets with matching cytokine profiles. Tc2, Tc17 and Tc22 type CD8+ T cell subsets, in contrast to classical cytotoxic Tc1 and Tc17+1 cells, possess a CD4 helper type alike phenotype characterized by absent cytotoxicity and SLAMF7 expression as well their ability to express CD40L upon activation. Their highly disparate homing patterns and unique TCR repertoire associates them to distinct immune responses as compared to those cytotoxic CD8+ T cells exert their role in. The dermal T cell gene expression signature and enrichment in psoriasis patients indicates that peripheral helper type CD8+ T cells represent a circulatory variant of skin resident cells.
2020-08-25 | GSE115103 | GEO
Project description:We show here that the T helper-fate is not fixed and that mature antigen-stimulated CD4 T cells can switch off Thpok expression and reactivate CD8- lineage genes. This unexpected plasticity results in the post-thymic termination of the T helper- program and the functional differentiation of distinct MHC class II restricted CD4 cytotoxic T lymphocytes Small intestine CD4 intraepithelial T lymphocytes from ThPOK-GFP reposter mice were isolated and sorted (FACS Aria) based on ThPOK and CD8aa expression. Cell were isolated either from non-experimental ThPOK-GFP reporter mice (WT) or after transfering CD4 naive T cells from ThPOK-GFP reporter mice to RAG-/-recipient animals (TR) as an experimental colitis model. Experimet was done in duplicate.
2012-12-10 | E-GEOD-42277 | biostudies-arrayexpress
Project description:We show here that the T helper-fate is not fixed and that mature antigen-stimulated CD4 T cells can switch off Thpok expression and reactivate CD8- lineage genes. This unexpected plasticity results in the post-thymic termination of the T helper- program and the functional differentiation of distinct MHC class II restricted CD4 cytotoxic T lymphocytes
2012-12-10 | GSE42277 | GEO
Project description:Cytotoxic CD8+ T cells can effectively kill target cells by producing cytokines, chemokines, and granzymes. Expression of these effector molecules is however highly divergent, and tools that identify and preselect CD8+ T cells with a cytotoxic expression profile are lacking. Human CD8+ T cells can be divided into IFN-γ– and IL-2–producing cells. Unbiased transcriptomics and proteomics analysis on cytokine-producing fixed CD8+ T cells revealed that IL-2+ cells produce helper cytokines, and that IFN-γ+ cells produce cytotoxic molecules. IFN-γ+ T cells expressed the surface marker CD29 already prior to stimulation. CD29 also marked T cells with cytotoxic gene expression from different tissues in single-cell RNA-sequencing data. Notably, CD29+ T cells maintained the cytotoxic phenotype during cell culture, suggesting a stable phenotype. Preselecting CD29-expressing MART1 TCR-engineered T cells potentiated the killing of target cells. We therefore propose that CD29 expression can help evaluate and select for potent therapeutic T cell products.
2020-03-20 | GSE125497 | GEO
Project description:Most people infected by EBV acquire specific immunity, which then controls latent infection throughout their life. Immune surveillance of EBV-infected cells by cytotoxic CD4+ T cells has been recognized; however, the molecular mechanism of generating cytotoxic effector T cells of the CD4+ subset remains poorly understood. Here we compared phenotypic features and the transcriptome of EBV-specific effector-memory CD4+ T cells and CD8+ T cells in mice and found that both T cell types show cytotoxicity and, to our surprise, widely similar gene expression patterns relating to cytotoxicity. Similar to cytotoxic CD8+ T cells, EBV-specific cytotoxic CD4+ T cells from human peripheral blood expressed T-bet, Granzyme B, and Perforin and upregulated the degranulation marker, CD107a, immediately after restimulation. Furthermore, T-bet expression in cytotoxic CD4+ T cells was highly correlated with Granzyme B and Perforin expression at the protein level. Thus, differentiation of EBV-specific cyto toxic CD4+ T cells is possibly controlled by mechanisms shared by cytotoxic CD8+ T cells. T-bet-mediated transcriptional regulation may explain the similarity of cytotoxic effector differentiation between CD4+ T cells and CD8+ T cells, implicating that this differentiation pathway may be directed by environmental input rather than T cell subset.
2022-08-26 | GSE206802 | GEO
Project description:Cytotoxic CD8+ T cells can effectively kill target cells by producing cytokines, chemokines and granzymes. Expression of these effector molecules is however highly divergent, and tools that identify and pre-select potent killer cells are lacking. Human CD8+ T cells can be divided into IFNGand IL-2 producing cells. Unbiased RNA-sequencing and proteomics analysis on cytokine-producing fixed CD8+ T cells revealed that IL-2+ T cells produce helper cytokines, and that IFNG+ T cells produce cytotoxic molecules. IFNG+ cytotoxic T cells expressed the surface marker CD29 already prior to stimulation. CD29 also marked T cells with cytotoxic gene expression from different tissues in single-cell RNA-sequencing data. Notably, the cytotoxic features of CD29+ T cells were maintained during cell culture, suggesting a stable phenotype. Pre-selecting CD29-expressing MART1 TCR-engineered T cells potentiated the killing of target cells. We therefore propose that selecting for CD29+ T cells could boost the anti-tumoral activity of T cell therapeutics.
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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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Project description:During a binary cell fate decision, a progeny silences the gene expression program associated with the alternative fate. Helper versus cytotoxic lineage decision in the thymus has been studied as a model for gene silencing of alternative lineage genes, including Cd4. While RUNX3 is required for the initiation of Cd4 silencing, it remains unknown how silenced states of Cd4 and other helper lineage genes are maintained. We show that the histone methyltransferase G9a is necessary for heritable silencing of Cd4 and other helper lineage genes in CD8 T cells. Despite normal Cd4 downregulation during the development, G9a-deficient CD8 T cells fail to maintain silencing of helper lineage genes when they repeatedly divide under non-inflammatory conditions. However, Cd4 depression is prevented during division driven by elevated TCR signaling and an inflammatory cytokine signaling. These results reveal the requirement for G9a in silencing of helper lineage genes in CD8 T cells and also suggest that CD8 T cells employ an alternative mechanism to maintain their cellular identity during immune responses.
2018-03-21 | GSE101730 | GEO
Project description:The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 or CoV-2) is the agent of a major global outbreak of respiratory tract disease known as COVID-19. CoV-2 infects the lungs and may cause several immune-related complications such as lymphocytopenia and cytokine storm which are associated with the severity of the disease and predict mortality. The mechanism by which CoV-2 infection may result in immune system dysfunction is not fully understood. Here we showed that CoV-2 infects human CD4+ T helper cells, but not CD8+ T cells. CoV-2 is found in the blood and bronchoalveolar lavage T helper cells of severe COVID-19 patients. We demonstrated that CoV-2 spike glycoprotein (S) (sCoV-2) directly binds to the CD4 co-receptor, which in turn mediates the entry of CoV-2 in T helper cells in a mechanism that also requires ACE2 and TMPRSS2. Once inside T helper cells, CoV-2 assembles viral factories, impairs cell function and may cause cell death. CoV-2 infected T helper cells express higher amounts of IL-10, which has been associated with viral persistence and disease severity. Thus, CD4-mediated CoV-2 infection of T helper cells may explain the poor adaptive immune response of many COVID-19 patients.
2023-07-28 | PXD020967 | Pride