期刊
IMMUNOLOGICAL REVIEWS
卷 249, 期 -, 页码 253-275出版社
WILEY
DOI: 10.1111/j.1600-065X.2012.01142.x
关键词
obesity; type 2 diabetes; T cell; B cell; human; immunometabolism
类别
资金
- 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
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据