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1,25-二羟维生素D3与牛结核病的发展

1,25-dihydroxyvitamin D3 and development of tuberculosis in cattle.

作者信息

Rhodes S G, Terry L A, Hope J, Hewinson R G, Vordermeier H M

机构信息

TB Research Group, Veterinary Laboratories Agency, Addlestone, Surrey KT15 3NB, United Kingdom.

出版信息

Clin Diagn Lab Immunol. 2003 Nov;10(6):1129-35. doi: 10.1128/cdli.10.6.1129-1135.2003.

Abstract

This report describes the presence and activity of 1,25-dihydroxyvitamin D3 (1,25-D3) in experimental bovine tuberculosis. Animals that went on to develop tuberculous lesions exhibited a rapid transient increase in serum 1,25-D3 within the first 2 weeks following infection with Mycobacterium bovis. 1,25-D3-positive mononuclear cells were later identified in all tuberculous granulomas by immunohistochemical staining of postmortem lymph node tissue. These results suggest a role for 1,25-D3 both at the onset of infection and in the development of the granuloma in these infected animals. Using a monoclonal antibody to the vitamin D receptor (VDR) as a VDR agonist, we confirmed that activation of the vitamin D pathway profoundly depresses antigen-specific, but not mitogenic, bovine peripheral blood T-cell responses (proliferation and gamma interferon production). Investigation of the mechanism of this suppression showed that the VDR antibody modified the expression of CD80 by accessory cells, such that a significant positive correlation between T-cell proliferation and accessory cell CD80 emerged.

摘要

本报告描述了1,25 - 二羟基维生素D3(1,25 - D3)在实验性牛结核病中的存在及活性。在感染牛分枝杆菌后的前两周内,出现结核病变的动物血清1,25 - D3迅速短暂升高。通过对死后淋巴结组织进行免疫组织化学染色,后来在所有结核性肉芽肿中均鉴定出1,25 - D3阳性单核细胞。这些结果表明1,25 - D3在这些感染动物的感染初期及肉芽肿形成过程中均发挥作用。使用针对维生素D受体(VDR)的单克隆抗体作为VDR激动剂,我们证实维生素D途径的激活会显著抑制抗原特异性而非促有丝分裂的牛外周血T细胞反应(增殖和γ干扰素产生)。对这种抑制机制的研究表明,VDR抗体改变了辅助细胞CD80的表达,使得T细胞增殖与辅助细胞CD80之间出现显著正相关。

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