Investigating the role of adipose tissue T cells in inflammation and insulin resistance

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Presentation Time: 11:30 AM - 12:45 PM
Poster Board Number: B191
Abstract ID: 5308

Presenting Author:
Hannah Guak , Postdoctoral fellow at Michigan Med., Univ. of Michigan

Abstract:

Obesity is associated with chronic inflammation, which is an important factor driving the pathogenesis of metabolic diseases such as cardiovascular disease and type 2 diabetes. Despite an enhanced inflammatory environment, immune responses against many infectious diseases are often impaired in people with obesity. In long-term obesity, adipose tissue T cells (ATT cells) adopt an exhaustion phenotype, which is commonly seen in settings where T cells are chronically stimulated, and is defined by loss of effector function, increased inhibitory receptor expression, and metabolic reprogramming. However, how ATT cell exhaustion develops is poorly understood. The central hypothesis of this study is that ATT cell exhaustion is induced by obesity to restrain inflammation and insulin resistance, thus contributing to impaired effector responses. We have previously identified the inhibitory receptor B and T cell lymphocyte attenuator (BTLA) as a marker induced in ATT cells by diet-induced obesity. Our results show that obese BTLA-deficient mice have reduced insulin sensitivity but normal weight gain, suggesting that BTLA plays a protective role in restraining obesity-induced insulin resistance independent of body mass. These data correlate with increased ATT cell activation potential, supporting a model where T cell exhaustion is protective in metabolic disease.