Basophils are inept at promoting human Th17 responses.

Basophils are the rare granulocytes and play an important role in the polarization of Th2 responses and protection against helminth parasites. In addition, basophils contribute to the pathogenesis of several diseases such as asthma, chronic allergy and lupus. Notably, Th17 cells are also implicated in the pathogenesis of these diseases suggesting that basophils support the activation and expansion of this subset of CD4(+) T cells. Therefore, we explored whether basophils promote the expansion of human Th17 cells. We show that basophils lack the capacity to expand Th17 cells and to induce the secretion of Th17 cytokines either directly or indirectly via antigen presenting cells such as monocytes. As human basophils lack HLA-DR and co-stimulatory molecules, their inability to confer T cell receptor- and co-stimulatory molecule-mediated signals to CD4(+) T cells might explain the lack of Th17 responses when memory CD4(+) T cells were co-cultured with basophils.