Invariant natural killer T cells (iNKT) cells can play an anti-inflammatory role and secrete the cytokine interleukin 10 (IL-10). IL-10 acts to inhibit signaling from inflammatory cytokines. Loss of iNKT cells has been implicated in cancer, autoimmune diseases, diabetes, and obesity. During early responses to immune challenge, iNKT cells provide help to B cells via two main pathways. Direct help from iNKT cells to B cells follows an innate pathway, while indirect help from iNKT cells to B cells follows an adaptive pathway. The specific interaction between B cells and iNKT cells within adipose tissue is not understood. Here, the interaction between iNKT cells and B cells within white adipose tissue and brown adipose tissue was examined using αGalCer, a potent stimulator of iNKT cells. In both brown and white adipose tissue, αGalCer stimulation resulted in an expansion of tissue-resident, IL-10 producing iNKT cells. However, tissue-resident B cells did not significantly increase in number or IL-10 production. Instead, a population of B220+CD19-CD1d+ lymphocytes were found to have an iNKT-dependent expansion in response to αGalCer. Our data suggests that iNKT cells provide indirect, adaptive help to B cells within both brown and white adipose tissue. These findings have implications in possible treatments for diabetes and obesity, as activated iNKT cells could be used to reduce tissue inflammation.