期刊
CELL REPORTS
卷 27, 期 2, 页码 514-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2019.03.030
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资金
- NIH [R56AI110682, R21AI117575, R01AI138337, P30DK56350]
- UNC-CH
- Pilot & Feasibility grant
- NCI Cancer Center Core Support Grant [P30CA016086]
- [R01-GM10974]
Obesity in humans is associated with poorer health outcomes after infections compared with non-obese individuals. Here, we examined the effects of white adipose tissue and obesity on T cell responses to viral infection in mice. We show that lymphocytic choriomeningitis virus (LCMV) grows to high titer in adipose tissue. Virus-specific T cells enter the adipose tissue to resolve infection but then remain as a memory population distinct from memory T cells in lymphoid tissues. Memory T cells in adipose tissue are abundant in lean mice, and diet-induced obesity further increases memory T cell number in adipose tissue and spleen. Upon re-challenge infection, memory T cells rapidly cause severe pathogenesis, leading to increases in lipase levels, calcification of adipose tissue, pancreatitis, and reduced survival in obese mice but not lean mice. Thus, obesity leads to a unique form of viral pathogenesis involving memory T cell-dependent adipocyte destruction and damage to other tissues.
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