Larsson P, Holmdahl R, Klareskog L
Department of Medical and Physiological Chemistry, University of Uppsala, Sweden.
J Cell Biochem. 1989 May;40(1):49-56. doi: 10.1002/jcb.240400106.
Resistance (low dose tolerance) to adjuvant arthritis was induced by intradermal immunization with 10 micrograms Mycobacterium tuberculosis administered 5 and 3 weeks before induction of arthritis. With the purpose of determining phenotypes of cells which participate in the maintenance of the induced resistance to adjuvant arthritis, tolerized rats were treated with two different anti-T-cell monoclonal antibodies. In tolerized rats, it was shown that anti-CD8 (OX8) antibodies, which caused an elimination of CD8+ lymphoid cells as determined by immunofluorescence analysis, made the rats responsive to an arthritogenic challenge with mycobacteria. Nine of 19 (47.4%) rats developed the disease as compared with 2 of 18 (11.1%) (P less than 0.05) in the control antibody-treated group. Also, in vivo treatment with anti-CD5 (OX19) monoclonal antibodies made the rats responsive to an arthritogenic challenge with mycobacteria. Nine of 15 (60%) anti-CD5-treated rats developed the disease as compared with 2 of 18 (11.1%) (P less than 0.01) rats in the control group. Immunofluorescence analysis performed after anti-CD5 treatment showed a reduction of staining of CD5+ cells as well as a down-regulation of the staining intensity of CD5 cell surface receptors on the remaining CD5+ cells. These data indicate that CD8+- as well as CD5+ cells participate in the maintenance of low dose tolerance to adjuvant arthritis.
在诱导关节炎前5周和3周，通过皮内注射10微克结核分枝杆菌来诱导对佐剂性关节炎的抗性（低剂量耐受性）。为了确定参与维持诱导的佐剂性关节炎抗性的细胞表型，用两种不同的抗T细胞单克隆抗体处理耐受大鼠。在耐受大鼠中，结果显示，通过免疫荧光分析确定可导致CD8 +淋巴细胞消除的抗CD8（OX8）抗体，使大鼠对分枝杆菌的致关节炎攻击产生反应。19只大鼠中有9只（47.4%）发病，而对照抗体处理组的18只大鼠中有2只（11.1%）发病（P<0.05）。此外，用抗CD5（OX19）单克隆抗体进行体内处理也使大鼠对分枝杆菌的致关节炎攻击产生反应。15只抗CD5处理的大鼠中有9只（60%）发病，而对照组的18只大鼠中有2只（11.1%）发病（P<0.01）。抗CD5处理后进行的免疫荧光分析显示CD5 +细胞染色减少，以及剩余CD5 +细胞上CD5细胞表面受体的染色强度下调。这些数据表明CD8 +细胞以及CD5 +细胞参与了对佐剂性关节炎低剂量耐受性的维持。
