iNKT cells operate within bi-directional cellular networks to alter the quality of immune responses through both cytokine production and direct cell-cell interactions. DCs are a part of this iNKT cell network, functioning as sentinels for microbial invasion and potent activators of iNKT cells. Following exposure of DCs to microbes or their PAMPs, iNKT cells are rapidly activated.  Once activated, iNKT cells in turn activate various DC effector functions, thereby enhancing downstream immune responses. During bacterial or fungal infection, we and others characterized iNKT cell-expressed IFNg and CD40L drive DC maturation and instruction, including enhanced antigen presentation, IL-12 secretion, and subsequent Th1 responses. As iNKT cells enhance immune responses in many inflammatory settings, we hypothesized that they might also modulate the cytosolic surveillance pathways involved in the assembly of inflammasomes and production of IL-1b, key regulators of innate and adaptive inflammatory responses. Here, we describe how iNKT cell cognate help directs DCs to produce high levels of IL-1b. The process requires the expression of CD1d by DCs and can occur after DC exposure to TLR agonists, even in the absence of exogenous lipid antigens. While iNKT cells trigger activation of the NLRP3 inflammasome in DCs, the majority of the IL-1β released is inflammasome-independent and occurs in the absence of cell death. Direct cell-cell interactions between iNKT cells and DCs drive early IL-1β through the NLRP3 inflammasome, and sustained IL-1b production through an inflammasome-independent mechanism. We are determining the molecular players that mediate this pathway, and its role in inflammation and host defense.