Activated Th17 clones can modulate human neutrophil responses through an IL-17–independent mechanism. Neutrophils were left untreated or cultured for 21 hours with supernatants from αCD3/αCD28-stimulated Th17 clones, in the presence or absence of neutralizing Abs against IL-17, IL-6, TNF-α, IFN-γ, GM-CSF, or TNF-α, IFN-γ, and GM-CSF in combination (or appropriate isotype control Abs), before evaluating their surface expression of CD66b (A) and CD11b (B) and their degree of apoptosis, as assessed by annexin V/PI staining (C) and by CD16 surface expression (D; n = 4). (A-B) Data are expressed as percentage of increase over the untreated condition. b vs a, P < .05; c vs b, P < .05; d vs b, P < .05.