The early innate responsiveness of the immune system is not only important for quick responses against pathogens but also to initiate and shape the subsequent adaptive response. In mice, repeated injections of IL-18, a product of inflammasome activation, give rise to a rapid inflammatory response that includes autoreactive antibody production. As IL-18 is elevated in both allergic and autoimmune inflammatory disease we investigated the origin of the B cell response and how it is regulated. We identified an influx of neutrophils to the spleen following IL-18 injections that promote the B cell response. It is known that NKT cells block this B cell response and we found that neutrophils activated NKT cells to upregulate the transcription factor GATA3 and FAS ligand. Increased expression of these molecules was abrogated in neutrophil-depleted mice. We found that FAS ligand expressed specifically by NKT cells was required to restrict B cell activation and autoantibody production. IL-18-injected mice which were depleted of neutrophils also had a dramatic increase in B cell activation, along with autoantibody production, indicating that neutrophils license NKT cells to regulate potentially harmful autoreactive B cell responses in inflammasome-driven inflammation. These findings are relevant for designing treatments of inflammatory diseases that often display lower NKT cells numbers in combination with elevated IL-18 levels.