Journal
IMMUNOLOGICAL REVIEWS
Volume 249, Issue -, Pages 253-275Publisher
WILEY
DOI: 10.1111/j.1600-065X.2012.01142.x
Keywords
obesity; type 2 diabetes; T cell; B cell; human; immunometabolism
Categories
Funding
- NIH [R21DK089270, 5R21DE021154, R56 DK090455]
- Leukemia and Lymphoma Society
- American Cancer Society
- Immunology Training Program [AI007309]
- Boston Area Diabetes Endocrinology Research Center Pilot Program
- Boston Nutrition Obesity Research Center [DK046200]
- Evans Center for Interdisciplinary Biomedical Research ARC on Obesity, Cancer and Inflammation at Boston University
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Obesity and Type 2 diabetes mellitus (T2D) are characterized by pro-inflammatory alterations in the immune system including shifts in leukocyte subset differentiation and in cytokine/chemokine balance. The chronic, low-grade inflammation resulting largely from changes in T-cell, B-cell, and myeloid compartments promotes and/or exacerbates insulin resistance (IR) that, together with pancreatic islet failure, defines T2D. Animal model studies show that interruption of immune cell-mediated inflammation by any one of several methods almost invariably results in the prevention or delay of obesity and/or IR. However, anti-inflammatory therapies have had a modest impact on established T2D in clinical trials. These seemingly contradictory results indicate that a more comprehensive understanding of human IR/T2D-associated immune cell function is needed to leverage animal studies into clinical treatments. Important outstanding analyses include identifying potential immunological checkpoints in disease etiology, detailing immune cell/adipose tissue cross-talk, and defining strengths/weaknesses of model organism studies to determine whether we can harness the promising new field of immunometabolism to curb the global obesity and T2D epidemics.
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