Abstract Body: High fat diet has long been implicated as a risk factor for obesity and other conditions associated with metabolic syndrome, including hypertension. The mechanism by which high fat diet increases risk of hypertension is likely multifactorial, but corresponding low-grade inflammation may play an important role. Low-grade inflammation associated with high fat diet is often accompanied by altered adipokine levels, including an increase in circulating chemerin. However, our understanding of the effects of chemerin and other adipokines on immune cells is limited. Thus, the purpose of these studies was to test the hypothesis that the adipokine chemerin promotes CD4 and CD8 T cell activation and cytokine secretion. To test this hypothesis, primary mouse splenocytes were treated with chemerin or vehicle 30 min prior to activation with a T cell-specific activator (anti-CD3/anti-CD28) for 24 h. T cell activation causes a rapid upregulation of cell surface proteins that are commonly used as experimental markers of activation. We found that chemerin did not impact the induction of the T cell activation markers, CD25, CD69, CD44, CD134, CD137 and CD154, in either CD4 or CD8 T cells. Likewise, we did not see a difference in the downregulation of CD62L, which is rapidly internalized by T cells following activation. Consistent with this, chemerin caused no difference in cytokine secretion by activated T cells. Specifically, the concentrations of IL-2, IL-17A, IFNγ, and TNFα were similar between groups. Overall, this study shows that the adipokine chemerin does not promote acute changes in activation or cytokine expression in primary mouse splenic T cells fully activated with anti-CD3/anti-CD28.