https://scholars.lib.ntu.edu.tw/handle/123456789/567814
標題: | Premature CD4+ T cell aging and its contribution to lymphopenia-induced proliferation of memory cells in autoimmune-prone non-obese diabetic mice | 作者: | Sheu T.-T. BOR-LUEN CHIANG Yen J.-H. Lin W.-C. |
公開日期: | 2014 | 出版社: | Public Library of Science | 卷: | 9 | 期: | 2 | 起(迄)頁: | e89379 | 來源出版物: | PLoS ONE | 摘要: | Lymphopenia-induced proliferation (LIP), a mechanism to maintain a constant number of T cells in circulation, occurs in both normal aging and autoimmune disease. The incidence of most autoimmune diseases increases with age, and premature CD4+ T cell aging has been reported in several autoimmune diseases. In this study, we tested the hypothesis that premature CD4+ T cell aging can cause autoimmune disease by examining whether premature CD4+ T cell aging exists and causes LIP in our mouse model. Non-obese diabetic (NOD) mice were used because, in addition to Treg defects, the LIP of T cells has been shown to plays a causative role in the development of insulin-dependent diabetes mellitus (IDDM) in these mice. We found that with advancing age, NOD mice exhibited an accelerated decrease in the number of CD4+ T cells due to the loss of na?ve cells. This was accompanied by an increase in the percentage of memory cells, leading to a reduced na?ve/memory ratio. In addition, both the percentage of CD28 + cells in CD4+ T cells and IL-2 production decreased, while the percentage of FAS+CD44+ increased, suggesting that NOD mice exhibit premature CD4+ T cell aging. This process preferentially contributed to LIP of memory cells. Therefore, our results suggest that premature CD4+ T cell aging underlies the development of IDDM in NOD mice. Given that CD28 and IL-2 play important roles in Treg function, the relationships between premature CD4+ T cell aging and lymphopenia as well as Treg defects in autoimmune-prone NOD mice are proposed. ? 2014 Sheu et al. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84896306996&doi=10.1371%2fjournal.pone.0089379&partnerID=40&md5=a3f5b413b97a432cdc1edece82985147 https://scholars.lib.ntu.edu.tw/handle/123456789/567814 |
ISSN: | 1932-6203 | DOI: | 10.1371/journal.pone.0089379 | SDG/關鍵字: | CD28 antigen; CD4 antigen; Fas antigen; Hermes antigen; interleukin 2; CD28 antigen; interleukin 2; animal cell; animal experiment; animal model; article; autoimmune disease; CD4 lymphocyte count; CD4+ T lymphocyte; cell loss; controlled study; cytokine production; diabetogenesis; disease predisposition; female; immunopathogenesis; insulin dependent diabetes mellitus; lymphocyte function; lymphocyte proliferation; lymphocytopenia; lymphopenia induced proliferation; memory cell; mouse; nonhuman; nonobese diabetic mouse; premature aging; regulatory T lymphocyte; animal; Bagg albino mouse; biosynthesis; CD4+ T lymphocyte; cell aging; cell proliferation; cytology; experimental diabetes mellitus; immunological memory; immunology; lymphocytopenia; obesity; Animals; Antigens, CD28; CD4-Positive T-Lymphocytes; Cell Aging; Cell Proliferation; Diabetes Mellitus, Experimental; Female; Immunologic Memory; Interleukin-2; Lymphopenia; Mice; Mice, Inbred BALB C; Mice, Inbred NOD; Obesity |
顯示於: | 醫學系 |
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