Unlocking tumor immune evasion: IL1RL1+ Treg cells and CAFs collaborate for immunotherapy resistance

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Unlocking tumor immune evasion: IL1RL1+ Treg cells and CAFs collaborate for immunotherapy resistance
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Researchers demonstrated that the crosstalk between IL1RL1+ regulatory T-cells (Treg) and cancer-associated fibroblasts (CAFs) drives the tissue repairing.

By Neha MathurAug 30 2023Reviewed by Lily Ramsey, LLM In a recent article published in the Science Advances Journal, researchers demonstrated that the crosstalk between IL1RL1+ regulatory T-cells and cancer-associated fibroblasts drives the tissue repairing and immunosuppressive CAF functional state, which is crucial for promoting tumorigenesis and maintaining cancer immune tolerance.

In case of tissue damage due to an environmental insult, tumor growth, or other diseases , IL-33 alerts several target immune cells expressing IL1RL1 , which initiates a cascade of immunological and pathological processes. AREG activates EGFR to promote the expression of tumor-growth factor-beta in CAFs, which likely causes immunosuppression in the TME. Notably, EGFR expression is predominant in CAFs but not Treg cells and other cell types in the TME. However, the precise mechanisms used by IL1RL1+ Treg cells to alter the TME and promote tumorigenesis are still elusive.

They performed paired single-cell ribonucleic acid sequencing and T-cell receptor sequencing of TCR-β+ T cells to analyze the immune cellular network in B16 and B16–IL-33 tumors on day nine post-tumor inoculation. Results The study data comprised 11,022 cells of three T-cell lineages: conventional T cells, cluster of differentiation 4+ Treg cells, and CD8+ T cells. B16–IL-33 versus B16 tumors showed increased Treg and CD8+ T cells and decreased Tconv cells accumulation.

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