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Fig. 2 | Journal for ImmunoTherapy of Cancer

Fig. 2

From: Resident memory T cells, critical components in tumor immunology

Fig. 2

Role of CD103 integrin in anti-tumor TRM functional activities. Engagement of TCR with specific peptide-MHC-I (p-MHC-I) complexes in the presence of TGF-β, abundant within the tumor microenvironment, induces expression of CD103 on the CD8+ T-lymphocyte surface. Phosphorylation of integrin-linked kinase (ILK) by TGFBR1, and its subsequent binding to the CD103 intracellular domain promotes inside-out signaling resulting in an increase in the affinity of the integrin for its ligand E-cadherin on tumor cells. Activated CD103 is recruited at the immune synapse formed between stimulated TRM cells and epithelial target cells; its interaction with E-cadherin triggers phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and the paxillin adaptor protein. Binding of phosphorylated (p)-paxillin to the αE (CD103) subunit tail triggers an outside-in signal that promotes CD8+ T-cell effector functions such as cytokine production and polarized release of cytotoxic granules, leading to TCR-mediated target cell death. Intra-tumoral TRM cells express very low levels of CD28 co-stimulatory receptor. Moreover, expression of LFA-1 on TIL is downregulated by TGF-β. Finally, cancer cells often downregulate expression of the LFA-1 ligand ICAM-1 to escape from immune effector cells

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