期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2002
卷号：99
期号：8
页码：5557-5560
DOI：10.1073/pnas.082100699
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：In addition to its role in calcium and phosphorous homeostasis, 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] appears to be a modulator of the immune system. Administration of 1,25-(OH)2D3 prevents disease in several autoimmune animal models, including experimental autoimmune encephalomyelitis (EAE). The vitamin D receptor is believed to mediate this activity. Among cells of the immune system, CD8+ T cells have the highest levels of the vitamin D receptor. Because CD8+ T cells have been implicated as both suppressors and effectors of the inflammation associated with multiple sclerosis and EAE, we examined the question of whether the 1,25-(OH)2D3 suppression of EAE occurs through a CD8+ T cell-dependent mechanism. To test this hypothesis, mice that are homozygous knockouts for the chain of the CD8 receptor and have been characterized as lacking functional CD8+ T cells (CD8+ -/-) were provided 1,25-(OH)2D3 in their diet before EAE induction. Although CD8+ -/- mice fed the same diet lacking 1,25-(OH)2D3 have a high incidence of EAE, EAE did not occur in CD8+ -/- mice fed the diet containing 1,25-(OH)2D3. We conclude that CD8+ T cells neither are needed nor do they play a role in the prevention of EAE by 1,25-(OH)2D3.
