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Cancer remains one of the leading causes of mortality worldwide, leading to increased interest in utilizing immunotherapy strategies for better cancer treatments. In the past decade, CD103+ T cells have been associated with better clinical prognosis in patients with cancer. However, the specific immune mechanisms contributing toward CD103-mediated protective immunity remain unclear. Here, we show an unexpected and transient CD61 expression, which is paired with CD103 at the synaptic microclusters of T cells. CD61 colocalization with the T cell antigen receptor further modulates downstream T cell antigen receptor signaling, improving antitumor cytotoxicity and promoting physiological control of tumor growth. Clinically, the presence of CD61+ tumor-infiltrating T lymphocytes is associated with improved clinical outcomes, mediated through enhanced effector functions and phenotype with limited evidence of cellular exhaustion. In conclusion, this study identified an unconventional and transient CD61 expression and pairing with CD103 on human immune cells, which potentiates a new target for immune-based cellular therapies.

Original publication

DOI

10.1038/s41590-024-01802-3

Type

Journal article

Journal

Nat Immunol

Publication Date

05/2024

Volume

25

Pages

834 - 846

Keywords

Animals, Humans, Mice, Antigens, CD, Apyrase, Cell Line, Tumor, Cytotoxicity, Immunologic, Integrin alpha Chains, Lymphocytes, Tumor-Infiltrating, Neoplasms, Receptors, Antigen, T-Cell, Signal Transduction, T-Lymphocytes, Cytotoxic