The function of T helper (TH) cells, the central organizers of adaptive immunity, is specified by the effector cytokines they produce. Regulation of TH cell cytokine secretion is not well understood and represents an important gap in our knowledge. In our preliminary studies, we found that in vitro, deficiency of membrane-associated nucleic acid binding protein (Mnab) led to profound defects in TH cell effector cytokine production. How Mnab regulates TH cell effector function is entirely unclear. We hypothesize that Mnab modulates stability of mRNAs encoding proteins in a common pathway that is critical in TH cell cytokine production. Our current data support a novel hypothesis that Mnab stabilizes mRNAs in the stress response-autophagy pathway that is required for secretory cells. In the proposed study, we will further understand how Mnab controls TH cell cytokine secretion and whether Mnab regulates TH cell function in disease models. Our studies will reveal a novel post-transcriptional control mechanism of TH cell effector function. Manipulation of the corresponding pathways may be of therapeutic benefit in human disease, such as autoimmune and inflammatory disorders.