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Publication : CD8(+) T cells are not necessary for 1 alpha,25-dihydroxyvitamin D(3) to suppress experimental autoimmune encephalomyelitis in mice.

First Author  Meehan TF Year  2002
Journal  Proc Natl Acad Sci U S A Volume  99
Issue  8 Pages  5557-60
PubMed ID  11929984 Mgi Jnum  J:76066
Mgi Id  MGI:2178496 Doi  10.1073/pnas.082100699
Citation  Meehan TF, et al. (2002) CD8+ T cells are not necessary for 1alpha,25-dihydroxyvitamin D3 to suppress experimental autoimmune encephalomyelitis in mice. Proc Natl Acad Sci U S A 99(8):5557-60
abstractText  In addition to its role in calcium and phosphorous homeostasis, 1alpha,25-dihydroxyvitamin D(3) [1,25-(OH)(2)D(3)] appears to be a modulator of the immune system. Administration of 1,25-(OH)(2)D(3) 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)(2)D(3) suppression of EAE occurs through a CD8(+) T cell-dependent mechanism. To test this hypothesis, mice that are homozygous knockouts for the alpha chain of the CD8 receptor and have been characterized as lacking functional CD8(+) T cells (CD8(+) -/-) were provided 1,25-(OH)(2)D(3) in their diet before EAE induction. Although CD8(+) -/- mice fed the same diet lacking 1,25-(OH)(2)D(3) have a high incidence of EAE, EAE did not occur in CD8(+) -/- mice fed the diet containing 1,25-(OH)(2)D(3). We conclude that CD8(+) T cells neither are needed nor do they play a role in the prevention of EAE by 1,25-(OH)(2)D(3).
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