University of California, San Francisco (UCSF)

Adipose Tissue Type 2 Immunity in Metabolic Health and Disease

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Over the past several decades there has been a remarkable population shift in body habitus, with over one-third of individuals in many high-income countries classified as obese, and rates of overweight and obese individuals rising worldwide. Obesity promotes local adipose tissue or ‘fat’ inflammation and is an early event in the development of insulin resistance and progression to diabetes. Our work has identified immune cells related to allergic/type 2immunity–including the recently identified group 2 innate lymphoid cells (ILC2) – that are abundant in lean, healthy adipose tissue and are protective in mouse models of obesity and diabetes. However, the regulation and function of these protective adipose tissue allergic immune cells are poorly understood. Our hypothesis is that adipose tissue signals are produced during normal tissue development and remodeling and recruit and support ILC2cells, promoting local and systemic metabolic health. In contrast, obesity-associated inflammatory cells and signals restrict adipose tissue ILC2 and the allergic ‘module’, contributing to the development of insulin resistance and diabetes. The objective of our work is to use a combination of 3D adipose tissue imaging, ‘omics’ approaches, and genetic tools in mouse models to understand the physiologic signals that regulate adipose tissue ILC2 cells and the allergic module, as well as the mechanistic contributions of ILC2 cells to metabolic health. This project is relevant to diabetes research because it has the potential to reveal novel cellular and molecular targets that can protect against obesity and the development of diabetes.