T cell specific eomesodermin knockout does not impact adipose senescence burden in middle aged mice 3073

Abstract Description   Cellular senescence is a state of permanent cell cycle arrest that results in inflammation. Eomes is a transcription factor involved in the transitioning of naïve T cells to memory T cells as well as T cell cytotoxicity. Eomes+ T cells play role in the clearance of senescent cells. Therefore, we sought to determine if 15-18 month old mice with T cell specific Eomes deletion exhibited an augmented senescence burden in the visceral adipose (VAT). We performed qPCR for senescence Cdkn2a(p16), Cdkn1a (p21), and Trp53 (p53) and inflammatory SASP genes Interleukin-6 (Il6), Tumor-necrosis factor-α (Tnfa), interferon-γ (Ifng), CCL2 (Ccl2), and CCL5 (Ccl5) in the VAT. VAT T cell number, phenotype, and senescence-associated β-galactosidase (SA-β-gal) activity were assessed by flow cytometry. We found no differences in the gene expression of p16, p21, p53, Il6, Tnfa, Ifng, Ccl2, or Ccl5. There are no significant differences in the median fluorescence intensity of SA-β-gal in T cells, B cells, endothelial cells, myeloid cells, and natural killer cells in the VAT. T cell Eomes-/- mice had a greater number of CD3+ and CD4+ T cells per gram of VAT. The number of CD8+ T cells tend to be greater in the Eomes-/-. Eomes-/- mice tended to have lower VAT weight. These results suggest that deleting the Eomes gene had no significant effect on cellular senescence, SASP factors, or inflammatory markers in the VAT but its absence may drive immune cell infiltration in VAT. Funding Sources NIH R01AG086447, AHA940023 Topic Categories Lymphocyte Differentiation and Peripheral Maintenance (LYM)