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TGF-b-dependent Lymphoid Tissue Residency of Stem-like T cells Limits the Response to Tumor Vaccine

ABSTRACT: TGF-b-dependent Lymphoid Tissue Residency of Stem-like T cells Limits the Response to Tumor Vaccine

PROVIDER: PRJNA736613 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14777158_1.fastq.gz	Fastqsanger.gz
	SRR14777158_2.fastq.gz	Fastqsanger.gz
	SRR14777159_1.fastq.gz	Fastqsanger.gz
	SRR14777159_2.fastq.gz	Fastqsanger.gz
	SRR14777160_1.fastq.gz	Fastqsanger.gz

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TGF-b-dependent Lymphoid Tissue Residency of Stem-like T cells Limits the Response to Tumor Vaccine

Project description:We report the transcriptional profiles of tumor-specific CD8+ T cells isolated from tumor draining lymph nodes (TDLN) and tumor following tumor vaccination in C57BL/6 mice. In addition, we included wild type (WT) and TGF-b receptor conditional knockout (Tgfbr2-/-) CD8+ T cells.

2021-06-11 | GSE176525 | GEO

Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency

Project description:Tissue-resident memory T (TRM) cells are integral to tissue immunity, persisting in diverse anatomical sites where they adhere to a common transcriptional framework. How these cells integrate distinct local cues to adopt the common TRM cell fate remains poorly understood. Here, we show that while skin TRM cells strictly require TGF-β for tissue residency, those in other locations utilize the metabolite retinoic acid (RA) to drive an alternative differentiation pathway, directing a TGF-β-independent tissue residency program in the liver and synergizing with TGF-β to drive the TRM cells in the small intestine.

2024-09-16 | GSE277120 | GEO

TGF-β-dependent lymphoid tissue residency of stem-like T cells limits response to tumor vaccine.

Project description:TGF-β signaling is necessary for CD8+ T cell differentiation into tissue resident memory T cells (TRM). Although higher frequency of CD8+ TRM cells in the tumor microenvironment is associated with better prognosis, TGF-β-blockade typically improves rather than worsens outcomes. Here we show that in a mouse melanoma model, in the tumor-draining lymph nodes (TDLN) rather than in the tumors themselves, stem-like CD8+ T cells differentiate into TRMs in a TGF-β and tumor antigen dependent manner. Following vaccination against a melanoma-specific epitope, most tumour-specific CD8+ T cells are maintained in a stem-like state, but a proportion of cells lost TRM status and differentiate into CX3CR1+ effector CD8+ T cells in the TDLN, which are subsequently migrating into the tumours. Disruption of TGF-β signaling changes the dynamics of these developmental processes, with the net result of improving effector CD8+ T cell migration into the tumours. In summary, TDLN stem-like T cells transiently switch from a TGF-β-dependent TRM differentiation program to an anti-tumor migratory effector development upon vaccination, which transition can be facilitated by targeted TGF-β blockade.

| S-EPMC9562983 | biostudies-literature

Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency [dnRA_Antag]

2024-09-16 | GSE277248 | GEO

Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency [dnRARa]

2024-09-16 | GSE277247 | GEO

TGF-b promotes stem-like T cells via enforcing their lymphoid tissue retention

Project description:Stem-like CD8+ T cells sustain the antigen-specific CD8+ T cell response during chronic antigen exposure. However, the signals that control the maintenance and differentiation of these cells are largely unknown. Here, we demonstrated that TGF-b was essential for the optimal maintenance of these cells and inhibited their differentiation into migratory effectors during chronic viral infection. Mechanistically, stem-like CD8+ T cells carried a unique expression pattern of a4 integrins (i.e., a4b1hi and a4b7lo) controlled by TGF-b. In the absence of TGF-b signaling, greatly enhanced expression of migration-related markers, including altered expression of a4 integrins led to enhanced egress of stem-like CD8+ T cells into the circulation accompanied by further differentiation into transitional states. Blocking a4 integrin significantly promoted their lymphoid tissue retention and therefore partially rescued the defective maintenance of Tcf-1+ subset in the absence of TGF-b signaling. Thus, TGF-b promotes the maintenance and inhibits the further differentiation of stem-like T cells at least partially via enforcing their lymphoid tissue residency.

2022-06-25 | GSE206646 | GEO

CXCR6 orchestrates brain CD8+ T cell residency and limits mouse Alzheimer’s disease pathology

Project description:CXCR6 orchestrates brain CD8+ T cell residency and limits mouse Alzheimer’s disease pathology

| PRJNA856707 | ENA

Runx3 programs CD8+ T cell residency in non-lymphoid tissues and tumours

Project description:Runx3 programs CD8+ T cell residency in non-lymphoid tissues and tumours

| PRJNA419960 | ENA

Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency

Project description:Retinoic acid and TGF-β orchestrate organ-specific programs of tissue-residency

| PRJNA1160824 | ENA

Comparative analysis reveals a role for TGF-β in shaping the residency-related transcriptional signature in tissue-resident memory CD8+ T cells

Project description:Tissue-resident CD8+ memory T (TRM) cells are immune cells that permanently reside at tissue sites where they play an important role in providing rapid protection against reinfection. They are not only phenotypically and functionally distinct from their circulating memory counterparts, but also exhibit a unique transcriptional profile. To date, the local tissue signals required for their development and long-term residency are not well understood. So far, the best-characterised tissue-derived signal is transforming growth factor-β (TGF-β), which has been shown to promote the development of these cells within tissues. In this study, we aimed to determine to what extent the transcriptional signatures of TRM cells from multiple tissues reflects TGF-β imprinting. We activated murine CD8+ T cells, stimulated them in vitro by TGF-β, and profiled their transcriptomes using RNA-seq. Upon comparison, we identified a TGF-β-induced signature of differentially expressed genes between TGF-β-stimulated and -unstimulated cells. Next, we linked this in vitro TGF-β-induced signature to a previously identified in vivo TRM-specific gene set and found considerable (>50%) overlap between the two gene sets, thus showing that a substantial part of the TRM signature can be attributed to TGF-β signalling. Finally, gene set enrichment analysis further revealed that the altered gene signature following TGF-β exposure reflected transcriptional signatures found in TRM cells from both epithelial and non-epithelial tissues. In summary, these findings show that TGF-β has a broad footprint in establishing the residency-specific transcriptional profile of TRM cells, which is detectable in TRM cells from diverse tissues. They further suggest that constitutive TGF-β signaling might be involved for their long-term persistence at tissue sites.

2019-01-23 | GSE125471 | GEO

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