Figure 2.
TME in EBV+ cHL and targets for adoptive T-cell immunotherapies. EBV infection is associated with various immune evasion strategies in cHL. (1) EBV infection induces JAK-STAT pathway activation, which leads to increased PD-L1 expression on HRS cells. (2) EBV-infected HRS cells express only the weakly immunogenic EBV antigens (EBNA1, LMP1, LMP2, and BARF1) in a type II latency pattern. (3) EBV+ HRS cells secrete IL-10, which inhibits CTLs directed at viral antigens. Adoptive immunotherapy strategies for EBV+ cHL include autologous and allogeneic EBV-specific CTLs and CAR T cells directed against viral antigens. JAK-STAT, Janus-associated kinase-signal transducer and activator of transcription; TCR, T-cell receptor.

TME in EBV+ cHL and targets for adoptive T-cell immunotherapies. EBV infection is associated with various immune evasion strategies in cHL. (1) EBV infection induces JAK-STAT pathway activation, which leads to increased PD-L1 expression on HRS cells. (2) EBV-infected HRS cells express only the weakly immunogenic EBV antigens (EBNA1, LMP1, LMP2, and BARF1) in a type II latency pattern. (3) EBV+ HRS cells secrete IL-10, which inhibits CTLs directed at viral antigens. Adoptive immunotherapy strategies for EBV+ cHL include autologous and allogeneic EBV-specific CTLs and CAR T cells directed against viral antigens. JAK-STAT, Janus-associated kinase-signal transducer and activator of transcription; TCR, T-cell receptor.

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