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

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

PROVIDER: PRJNA691511 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13416103_1.fastq.gz	Fastqsanger.gz
	SRR13416103_2.fastq.gz	Fastqsanger.gz
	SRR13416104_1.fastq.gz	Fastqsanger.gz
	SRR13416104_2.fastq.gz	Fastqsanger.gz
	SRR13416105_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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.

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. [CD4 T cells]

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

| PRJNA691510 | ENA

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:A key unknown of the functional space in tumor immunity is whether CD4 T cells depend on intratumoral MHCII cancer antigen recognition. MHCII-expressing, antigen-presenting cancer-associated fibroblasts (apCAFs) have been found in breast and pancreatic tumors and are considered to be immunosuppressive. This analysis shows that antigen-presenting fibroblasts are frequent in human lung non-small cell carcinomas, where they seem to actively promote rather than suppress MHCII immunity. Lung apCAFs directly activated the TCRs of effector CD4 T cells and at the same time produced C1q, which acted on T cell C1qbp to rescue them from apoptosis. Fibroblast-specific MHCII or C1q deletion impaired CD4 T cell immunity and accelerated tumor growth, while inducing C1qbp in adoptively transferred CD4 T cells expanded their numbers and reduced tumors. Collectively, we have characterized in the lungs a subset of antigen-presenting fibroblasts with tumor-suppressive properties and propose that cancer immunotherapies might be strongly dependent on in situ MHCII antigen presentation.

| 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

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

Transcriptome data of MHCII-high and MHCII-low hematopoietic stem cells of middle-aged mice

Project description:Analysis of MHCII-high (MHCII-hi) and MHCII-low (MHCII-lo) hematopoietic stem cells (Lineage-Sca-1+c-Kit+CD150+Flt3-CD48-). The two population of hematopoietic stem cell (HSC) were purified from the bone marrow of 12 months old (12 mo) mice. Results provide insight into the role of MHCII in HSC.

2023-08-08 | GSE211206 | GEO

Transcriptome data of MHCII-high and MHCII-low hematopoietic stem cells of mice under homeostasis

Project description:Analysis of MHCII-high (MHCII-hi) and MHCII-low (MHCII-lo) hematopoietic stem cells (Lineage-Sca-1+c-Kit+CD150+Flt3-CD48-). The two population of hematopoietic stem cell (HSC) were purified from the bone marrow of 5 months old WT mice (Ctrl). Results provide insight into the role of MHCII in HSC.

2023-08-08 | GSE211203 | GEO

Transcriptome data of MHCII-high and MHCII-low hematopoietic stem cells of mice exposed to irradiation

Project description:Analysis of MHCII-high (MHCII-hi) and MHCII-low (MHCII-lo) hematopoietic stem cells (Lineage-Sca-1+c-Kit+CD150+Flt3-CD48-). The two population of hematopoietic stem cell (HSC) were purified from the bone marrow of mice at 3 months post 5 Gy total body irradiation (IR). Results provide insight into the role of MHCII in HSC.

2023-08-08 | GSE211205 | GEO

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