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Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts. [CD4 T cells]

ABSTRACT: Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts. [CD4 T cells]

PROVIDER: PRJNA691510 | ENA |

REPOSITORIES: ENA

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Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts.

Project description:Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts.

| PRJNA691506 | ENA

Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts. [CAF]

Project description:Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts. [CAF]

| PRJNA691511 | ENA

Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts. [CAF]

Project description:A key unknown of the functional space in tumor immunity is whether physiologically relevant cancer antigen presentation occurs solely in draining lymph nodes versus tumors. Professional antigen presenting cells, i.e. the dendritic cells, are scarce and immature within tumors, greatly outnumbered by MHCII expressing non-hematopoietic cells, such as antigen-presenting cancer-associated fibroblasts (apCAFs). We hypothesized that after their exit from tumor-draining lymph nodes T cells depend on a second wave of antigen presentation provided in situ by structural cells. We show that dense apCAF regions in human lung tumors define hot immunological spots with increased numbers of CD4 T cells. The transcriptomic profile of human lung apCAFs aligned to that of pancreatic apCAFs across mice and humans and were both enriched for alveolar type II genes, suggesting an epithelial origin. Mechanistically, human apCAFs directly activated the TCRs of adjacent effector CD4 T cells and at the same time produced high levels of c1q, which acted on surface c1qbp on T cells to rescue them from apoptosis. Fibroblast-specific deletion of MHCII in mice impaired local MHCII immunity and accelerated tumor growth, while inducing c1qbp overexpression in adoptively transferred T cells expanded their numbers within tumors and reduced tumour burden. Collectively, our work shows that tumor T cell immunity post lymph node exit requires peripheral antigen presentation by a subset of CAFs and proposes a new conceptual framework upon which effective cancer immunotherapies can be built.

2021-12-13 | GSE164653 | GEO

Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts. [CD4 T cells]

2021-12-13 | GSE164659 | GEO

Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts.

Project description: Not available

| S-EPMC8764966 | biostudies-literature

Lung tumor MHCII immunity depends on in situ antigen presentation by fibroblasts.

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-13 | GSE164660 | GEO

HLA-DM allotypes - Distinct editing functions of natural HLA-DM allotypes impact antigen presentation and CD4+ T cell activation

Project description:Major Histocompatibility Complex of Class II (MHCII) antigen presentation is a key event of adaptive immunity. HLA-DM favors the presentation of kinetically stable peptide-MHCII complexes but does not bind peptides itself and exhibits only a low degree of polymorphism. To date, no evidence for altered function of DM due to natural variations has been reported. We define the presence of DM haplotypes in human populations covered by the 1000 Genomes Project and probe their activity in antigen presentation assays. Our results indicate a clear linkage between DMA*0103 and DMB*0107 never reported before. Thehe corresponding heterodimer features a distinct activity profile when compared to the most frequent allotype (DMA*0101-DMB*0101). In vitro experiments demonstrate a broader pH activity profile for the new allotype, explaining its characteristic cellular function. Together, our results suggest that natural variations of DM have important consequences for an individual’s adaptive immune response.

2018-10-31 | PXD009791 | Pride

MHC class II antigen presentation by tumoral lymphatics is required for tumor specific signature and suppressive functions of Tregs

Project description:A number of solid malignancies triggers lymphangiogenesis, facilitating metastasis. Recent studies further indicate that tumor-associated lymphatic vessels significantly contribute to the generation of an immunosuppressive tumor microenvironment. Here, we have investigated the ability of tumor-associated lymphatic endothelial cells (LECs) to function as MHC class II restricted antigen-presenting cells in the regulation of anti-tumor immunity. Using murine models of lymphangiogenic tumors engrafted under the skin, we show that tumor LECs upregulate MHCII and the MHCII antigen processing machinery, and promote Treg expansion ex vivo. Using mice with a LEC-restricted lack of MHCII expression, we demonstrate that tumor growth is severely impaired, whereas tumor-infiltrating T effector cells are increased. Reduction of tumor growth and reinvigoration of tumor-specific T cell responses both result from alterations of the tumor-infiltrating regulatory T cell (Treg) transcriptome and phenotype. Treg suppressive functions are consequently profoundly altered in tumors lacking MHCII in LECs. No difference in effector T cell responses or Treg phenotype and functions were observed in tumor-draining lymph nodes, indicating that MHCII restricted antigen presentation by LECs is required locally in the tumor microenvironment (TME) to confer potent suppressive functions to Tregs. Altogether, our study advocates a role for MHCII-restricted antigen-presenting tumor LECs that function as a local brake, dampening tumor T cell immunity and promoting intratumoral Treg suppressive functions.

2024-03-01 | GSE168609 | GEO

Oligomeric human Aβ1-42 inhibits antigen presentation

Project description:Oligomeric human Aβ1-42 inhibits antigen presentation

| PRJNA563674 | ENA

Microarray expression analysis depicting MHCII-dependent features of FOXP3-expressing CD4 T regulatory cells

Project description:Analysis comparing K14 and MCHII+/- Tregs. The hypothesis was that the lack of MHCII+/- in the spleen and intestine would result in a large shift in K14 Treg gene expression away from an activated and effector phenotype. Results demonstrate how a lack of MHCII-antigen presentation in the small intestine, where Tregs exhibit an effector penotype, does not greatly reduce effector features of T regulatory cells in K14 mice.

2023-11-15 | GSE226193 | GEO

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