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Title: Essential role of CD11a in CD8+ T-cell accumulation and activation in adipose tissue

Author
item JIANG, ERLIE - Baylor College Of Medicine
item PERRARD, XIAOYUAN - Baylor College Of Medicine
item YANG, DONGLIN - Baylor College Of Medicine
item KHAN, ILVIRA - Baylor College Of Medicine
item PERRARD, JERRY - Baylor College Of Medicine
item SMITH, CLIFTON - Children'S Nutrition Research Center (CNRC)
item BALLANTYNE, CHRISTIE - Baylor College Of Medicine
item WU, HUAIZHU - Baylor College Of Medicine

Submitted to: Arteriosclerosis Thrombosis and Vascular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/15/2013
Publication Date: 1/1/2014
Citation: Jiang, E., Perrard, X.D., Yang, D., Khan, I.M., Perrard, J.L., Smith, C.W., Ballantyne, C.M., Wu, H. 2014. Essential role of CD11a in CD8+ T-cell accumulation and activation in adipose tissue. Arteriosclerosis Thrombosis and Vascular Biology. 34(1):34-43.

Interpretive Summary: Some types of white blood cells participate in the inflammation that occurs in fat tissues in obese individuals and in the diseases that arise from obesity. This study examines one special type of white blood cell called CD8 T cells in mice fed a high fat and high carbohydrate diet, and analyzes some of the proteins that are necessary for these cells to increase in fat tissues and to promote inflammation that leads to diabetes. The results show that two of these proteins called CD18 and CD11a act to allow the CD8 T cells to gain entrance to fat tissues and promote inflammation. This new information will be helpful in designing therapies for the obesity-related inflammation that promotes complications of obesity such as diabetes.

Technical Abstract: T-cells, particularly CD8+ T-cells, are major participants in obesity-linked adipose tissue inflammation. We examined the mechanisms of CD8+ T-cell accumulation and activation in adipose tissue and the role of CD11a, a beta2 integrin. CD8+ T-cells in adipose tissue of obese mice showed activated phenotypes with increased proliferation and interferon-gamma expression. In vitro, CD8+ T-cells from mouse adipose tissue displayed increased interferon-gamma expression and proliferation to stimulation with interleukin-12 and interleukin-18, which were increased in obese adipose tissue. CD11a was upregulated in CD8+ T-cells in obese mice. Ablation of CD11a in obese mice dramatically reduced T-cell accumulation, activation, and proliferation in adipose tissue. Adoptive transfer showed that CD8+ T-cells from wild-type mice, but not from CD11a-deficient mice, infiltrated into adipose tissue of recipient obese wild-type mice. CD11a deficiency also reduced tumor necrosis factor-a–producing and interleukin-12–producing macrophages in adipose tissue and improved insulin resistance. Combined action of cytokines in obese adipose tissue induces proliferative response of CD8+ T cells locally, which, along with increased infiltration, contributes to CD8+ T-cell accumulation and activation in adipose tissue. CD11a plays a crucial role in adipose tissue inflammation by participating in T-cell infiltration and activation.