Cantorna M T, Woodward W D, Hayes C E, DeLuca H F
Department of Biochemistry, University of Wisconsin-Madison, College of Agricultural and Life Sciences 53706, USA.
J Immunol. 1998 Jun 1;160(11):5314-9.
Previously we demonstrated that 1,25-dihydroxyvitamin D3 blocks the progression of relapsing encephalomyelitis. We now propose that 1,25-dihydroxyvitamin D3 blocks these autoimmune symptoms by stimulating the differentiation and/or function of cells that inhibit the encephalitogenic process. To support this belief, we have found that 1,25-dihydroxyvitamin D3 administration to mice increases IL-4 transcripts by 3- to 25-fold and TGF-beta 1 transcripts by 4- to 24-fold. Similarly, IL-4 and TGF-beta 1 transcripts were higher in the central nervous system of 1,25-dihydroxyvitamin D3-treated mice compared with controls. The number of cells recoverable from the lymph nodes of 1,25-dihydroxyvitamin D3-treated mice was only 50% that of controls. Overall, 1,25-dihydroxyvitamin D3 treatment causes a net loss in the total number of lymphocytes while the number of IL-4 and TGF-beta 1 transcripts increased. The systemic and local increase in the expression of these two anti-inflammatory cytokines by 1,25-dihydroxyvitamin D3 may be responsible for the ability of this drug to block encephalomyelitis.
此前我们证明，1,25 - 二羟基维生素D3可阻断复发性脑脊髓炎的进展。我们现在提出，1,25 - 二羟基维生素D3通过刺激抑制致脑炎过程的细胞的分化和/或功能来阻断这些自身免疫症状。为支持这一观点，我们发现给小鼠施用1,25 - 二羟基维生素D3可使IL - 4转录本增加3至25倍，使TGF - β1转录本增加4至24倍。同样，与对照组相比，1,25 - 二羟基维生素D3处理的小鼠中枢神经系统中的IL - 4和TGF - β1转录本更高。从1,25 - 二羟基维生素D3处理的小鼠淋巴结中可回收的细胞数量仅为对照组的50%。总体而言，1,25 - 二羟基维生素D3处理导致淋巴细胞总数净减少，而IL - 4和TGF - β1转录本数量增加。1,25 - 二羟基维生素D3引起的这两种抗炎细胞因子表达的全身和局部增加可能是该药物阻断脑脊髓炎能力的原因。
