Accordingly, LAYN deletion resulted in attenuated LFA-1-dependent cellular adhesion. On a molecular level, layilin colocalized with integrin αLβ2 (LFA-1) on T cells, and cross-linking layilin promoted the activated state of this integrin. Congruently, gene editing of LAYN in human CD8+ T cells reduced direct tumor cell killing ex vivo. Lineage-specific deletion of layilin on murine CD8+ T cells reduced their accumulation in tumors and increased tumor growth in vivo. Here, we report that layilin, a C-type lectin domain-containing membrane glycoprotein, is selectively expressed on highly activated, clonally expanded, but phenotypically exhausted CD8+ T cells in human melanoma. However, the mechanisms by which T cells remain poised to kill cancer cells despite expressing high levels of inhibitory receptors are unknown. Tumor-infiltrating CD8+ T cells mediate antitumor immune responses.
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