Mia Bodnar-Cohen
Pronouns: she/her/hers
Research Mentor(s): Carey Lumeng
Research Mentor School/College/Department: Pediatrics, Physiology / Medicine
Program: UROP
Session: Session 2 (10:00am – 10:50am)
Authors: Mia Bodnar-Cohen, Hannah Guak
Abstract
Obesity leads to major health issues as a result of chronic inflammation, including metabolic diseases, such as type 2 diabetes, and impaired immune responses, such as worsened COVID-19 outcomes. Recent studies have indicated that with long-term obesity comes adipose tissue T cell exhaustion (Porsche et al, 2021 and Hasty lab paper Cottam et al, 2022), which results in T cells’ inability to perform their immunoregulatory functions. Glucocorticoids are small lipid hormones known to inhibit T cell-mediated immune responses (Acharya et al, Immunity 2020). Previous studies have discovered that endogenous glucocorticoid levels in adipose tissue are increased with human obesity (Rask et al, J. Clin. Endocrinol. Metab. 2001). However, the link between these distinct research areas has not yet been examined. To investigate the effects of glucocorticoid signaling on adipose tissue T cell exhaustion, we bred mice with a T cell-specific deficiency of the glucocorticoid receptor and genotyped these mice using polymerase chain reaction (PCR), gel electrophoresis, and RT-qPCR. We crossed mice that have loxP sites flanking the glucocorticoid receptor Nr3c1 with mice that express Cre recombinase under the Lck or Cd4 promoters to target T cells specifically. In addition, we have optimized qPCR using Taqman probes to genotype mice expressing Cre recombinase under the Lck promoter. Next, we plan on examining gene expression using qPCR of metabolic and inflammatory factors in adipose tissue from transgenic mice. With a better understanding of how adipose tissue T cell exhaustion is regulated, we can determine what steps can be taken to improve the health of the immune system in obese individuals.
