IL-36/IL-36R signaling promotes CD4

Background: Inflammatory bowel disease (IBD) is a multifactorial, chronic disease that affects approximately 1.5 million people in the United States. Several important factors are implicated in the pathogenesis of IBD, one factor being dysregulation of the immune system. This dysregulation results in the accumulation and stimulation of innate and adaptive immune cells, and subsequent release of soluble factors, including pro-inflammatory cytokines. One of these cytokines is a member of the IL-36 cytokine family, IL-36γ, which is overexpressed in human IBD and experimental models of colitis. In this study, we explored the role of IL-36γ in promoting CD4 Methods: Spleens and lymph nodes were collected from wild-type and IFNγ Results: Our results demonstrate that IL-36γ stimulation of naive CD4 Conclusion: These data not only suggest that IL-36γ is a regulator of a pro-inflammatory cytokine network involving IFNγ and TNFα but also highlights the importance of targeting IL-36γ and IFNγ as therapeutic approaches. Our studies have broad implications in relation to targeting specific cytokines in human IBD.