Abstract

Inflammation is necessary for immune defense against pathogens and a functional antitumor immune response, but chronic inflammation promotes tumor growth and enables tumors to escape from immune-mediated destruction. Recently, we and others demonstrated that deficiency of IL1β strongly favors antitumor immunity, and multiple clinical trials involving antibody mediated IL1β blockade in multiple cancers are underway. The mechanism, however, remains obscure. We demonstrated that intact IL1α signaling was required for IL1β blockade-induced antitumor immunity, leading to the hypothesis that its interaction with the IL1 type I receptor (IL1R1) and subsequent signaling was required for the antitumor immune response.

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