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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

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

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE132297 | GEO | 2021/05/03

REPOSITORIES: GEO

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Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

Project description:Follicular regulatory T cells (TFR cells) and their functional role in cancer have been completely disregarded so far. Our data identify that as a critical oversight, as these cells account for a substantial proportion of tumor-infiltrating CD4+ T cells

2022-06-01 | GSE145691 | GEO

Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [mouse]

2021-05-03 | GSE132296 | GEO

Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [human]

2021-05-03 | GSE132295 | GEO

Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

Project description:Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

| PRJNA607958 | ENA

Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

Project description:Intratumoral TFR cells curtail anti-PD-1 treatment efficacy

| PRJNA547551 | ENA

Intratumoral follicular regulatory T cells curtail anti-PD-1 treatment efficacy.

Project description:Immune-checkpoint blockade (ICB) has shown remarkable clinical success in boosting antitumor immunity. However, the breadth of its cellular targets and specific mode of action remain elusive. We find that tumor-infiltrating follicular regulatory T (TFR) cells are prevalent in tumor tissues of several cancer types. They are primarily located within tertiary lymphoid structures and exhibit superior suppressive capacity and in vivo persistence as compared with regulatory T cells, with which they share a clonal and developmental relationship. In syngeneic tumor models, anti-PD-1 treatment increases the number of tumor-infiltrating TFR cells. Both TFR cell deficiency and the depletion of TFR cells with anti-CTLA-4 before anti-PD-1 treatment improve tumor control in mice. Notably, in a cohort of 271 patients with melanoma, treatment with anti-CTLA-4 followed by anti-PD-1 at progression was associated with better a survival outcome than monotherapy with anti-PD-1 or anti-CTLA-4, anti-PD-1 followed by anti-CTLA-4 at progression or concomitant combination therapy.

| S-EPMC8434898 | biostudies-literature

Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [human]

Project description:Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [human]

| PRJNA547554 | ENA

Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [mouse]

Project description:Intratumoral TFR cells curtail anti-PD-1 treatment efficacy [mouse]

| PRJNA547567 | ENA

Anti-PD-L1 Lead-in Before MAPKi Combination Maximizes Anti-Tumor Efficacy and Immunity.

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

2021-08-19 | GSE177902 | GEO

Tumor-Induced Erythroid Precursor-Differentiated Myeloid Cells Mediate Immunosuppression and Curtail Anti-PD-1/PD-L1 Treatment Efficacy

Project description:Despite the unprecedented success of immune checkpoint inhibitors (ICIs) as anti-cancer therapy, it remains a prevailing clinical need to identify additional mechanisms underlying ICI therapeutic efficacy and potential drug resistance. Here, using lineage tracking in cancer patients and tumor-bearing mice, we demonstrate that erythroid progenitor cells lose their developmental potential and switch to the myeloid lineage. Single-cell transcriptome analyses reveal that, notwithstanding quantitative differences in erythroid gene expression, erythroid differentiated myeloid cells (EDMCs) are transcriptionally indistinguishable from their myeloid-originated counterparts. EDMCs possess multifaceted machinery to curtail T cell-mediated anti-tumor responses. Consequently, EDMC content within tumor tissues is negatively associated with T cell inflammation for the majority of solid cancers; moreover, EDMC enrichment, in accordance with anemia manifestation, is predictive of poor prognosis in various cohorts of patients undergoing ICI therapy. Together, our findings reveal a feed-forward mechanism by which tumors exploit anemia-triggered erythropoiesis for myeloid transdifferentiation and immunosuppression.

2022-04-30 | GSE201715 | GEO

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