AuthOr’s VIew AuthOr’s VIew

Renal cell carcinoma (RCC) exhibit a prominent immune cell infiltrate consist-ing of T cells, natural killer (NK) cells, dendritic cells (DCs) and macrophages. Intratumoral CD8+ T and NK cells are differentiated effector cells with lytic granules.1 Moreover, some CD8+ T cells express a tumor-reactive T-cell receptor (TCR)2 and mediate antitumor reactivity when analyzed ex vivo following exposure to interleukin (IL)-2.1 A high frequency of NK cells among the lymphocytic infiltrate seems to predict a better prognosis.3 Still, tumors grow despite the infiltration of potentially tumor-reactive cytotoxic effec-tor cells indicating that their antitumor activity is compromised within the tumor microenvironment. Using immune histology and ex vivo analysis of tumor-infiltrating leukocytes (TILs), we identified alterations in RCC-infiltrating T cells, NK cells and DCs that may be relevant for the loss of local immune competence and ensuing in tumor immunoescape.1,4 DCs are central regulators of immune responses with the capacity to induce immunity or tolerance depending on their differentiation state. Thus, targeting this cell population would constitute an effec-tive means for tumors to alter the immune Intratumoral alterations of dendritic-cell differentiation and CD8+ T-cell anergy are immune escape mechanisms of clear cell renal cell carcinom