The effects of TNF-a on T cell homeostasis in obese and diabetic mice

Obesity is a growing epidemic in the United States that leads to many complications, including exacerbation of colitis and diminished immune response. Obesity increases levels of TNF-a systemically, causing chronic inflammation. This inflammation suppresses gd-T lymphocytes in epithelial tissues, which play key roles in tissue repair through the release of growth factors and activation of macrophages. Our previous research shows that blocking TNF-a for four days prior to wounding can help improve T cell function. This research focuses on how TNF-a affects intestinal epithelial T cells, splenic T lymphocyte homeostasis, and TNF-a function in obesity. Our study used mice deficient in TNFR1 and TNFR2 to investigate the changes imposed by an absence of TNF-a signaling. Data collected from splenic T cells and small intestine were compared to provide us with insight to the local and peripheral effects of mice with and without TNFR1 and TNFR2. Our current data suggest that TNFR1 and TNFR2 deficient obese mice show a decreased number of splenic T lymphocytes. Wound repair remains dysfunctional in obese mice even in the absence of TNFR1 and 2 suggesting epithelial T cells require TNFR signaling for normal function. The results thus far suggest that TNF-a is an essential cytokine in maintaining the homeostasis and function of T lymphocytes in obese mice. Further research will be conducted involving TNF-a and its receptors on the immune cells of obese and diabetic individuals.