Adoptively transferred Th17 cells cooperate with host B cells to achieve durable tumor immunity

This is the authors' abstract. We don't add key points for this paper.

CD4 + T helper cells play an important role in adoptive T cell therapy (ACT) success, but it remains unclear which subset is most therapeutic and how they eliminate tumors. We find that tumor-specific Th17 cells eradicate melanoma more effectively than other CD4 + subsets and protect against distant metastases by unique orchestration of host immunity. Donor Th17 cells require host B cells —but not T cells— for tumor regression. Th17 cells induce B cell proliferation, activation, and differentiation, while B cells augment Th17 cell polyfunctionality by enhancing IL-21 production. Th17 and B cells colocalize in lymphoid tissues, where Th17 cells induce germinal centers and tumor-reactive antibodies via IL-21 production and CD40L costimulation. Furthermore, these tumor-specific antibodies provide partial protection against tumor challenge. Herein, we reveal that adoptively transferred Th17 cells cooperate with B cells to drive sustained immunity, demonstrating a role for endogenous B cell responses in effective CD4 + ACT. • Host B cells are required for tumor control by adoptively transferred Th17 cells • Th17 cells promote host B cell proliferation, maturation, and antibody production • IL-21 and CD40L are required for B cell responses and long-lasting tumor immunity • Th17 cells elicit tumor-specific IgG that limits metastatic tumor spread Cole et al. report that adoptively transferred, tumor-specific Th17 cells engage host B cells and drive B cell proliferation and differentiation. These Th17 cells require B cells for sustained immunity and elicit a potent humoral response that can protect against tumors.