T-cell subsets within the Hodgkin lymphoma tumor microenvironment tip the balance away from tumor immunity. In comparison to reactive lymph nodes and tonsils, T cells infiltrating cHL tumors have marked expansions in T-cell subsets that can suppress tumor-specific killing (Treg cells, PD-1 low/negative; >10-fold expanded) and EM CD4+ T cells with PD-1 intermediate/high expression (Th1 EM, Th1 TEMRA; >fivefold expanded), rendering them sensitive to the suppressive effects of the high levels of PD-L1 expressed by HRS cells. The effectiveness of PD-1 blockade in cHL may rely on the release of these effector CD4+ T-cell populations from PD-L1-mediated suppression, achieving tumor control presumably via class II MHC-mediated cytotoxicity. CM, central memory. The figure has been adapted from Figure 7C in the article by Cader et al that begins on page 825.

T-cell subsets within the Hodgkin lymphoma tumor microenvironment tip the balance away from tumor immunity. In comparison to reactive lymph nodes and tonsils, T cells infiltrating cHL tumors have marked expansions in T-cell subsets that can suppress tumor-specific killing (Treg cells, PD-1 low/negative; >10-fold expanded) and EM CD4+ T cells with PD-1 intermediate/high expression (Th1 EM, Th1 TEMRA; >fivefold expanded), rendering them sensitive to the suppressive effects of the high levels of PD-L1 expressed by HRS cells. The effectiveness of PD-1 blockade in cHL may rely on the release of these effector CD4+ T-cell populations from PD-L1-mediated suppression, achieving tumor control presumably via class II MHC-mediated cytotoxicity. CM, central memory. The figure has been adapted from Figure 7C in the article by Cader et al that begins on page 825.

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