Diabetes and cancer currently represent two of the largest healthcare burdens and leading causes of death in the United States. Our work, in addition to others, has shown the fascinating dichotomous roles of the immune system in these diseases. While we have demonstrated that the immune system limits cancer formation through activation of circulating lymphocytes called Natural Killer (NK) cells, unrestrained activation of NK cells and adipose-resident innate lymphoid type 1 (ILC1) cells during diet-induced obesity can increase adipose tissue inflammation, leading to a pre-diabetic state. Therefore, our current projects seek to understand the upstream activating signals that are induced during cancer and obesity, as well as the fundamental contributions of tissue-resident vs circulating lymphocytes in these diseases. Understanding the precise cellular and molecular mechanisms used by the immune system to prevent or promote pathology in these contexts will create potential therapies for the treatment of cancer and type II diabetes.
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