Fujisawa H, Nishimura T, Inaba M, Ikehara S
Research Laboratories, Nippon Shinyaku Pharmaceutical Co., Ltd, Kyoto, Japan.
Int J Immunopharmacol. 1995 Jul;17(7):611-7. doi: 10.1016/0192-0561(95)00044-3.
We examined the effects of actarit, a new antirheumatic drug, on antibody production after LPS stimulation in mice. Actarit did not affect the proliferative response of B-cells stimulated with LPS or anti-mouse mu-chain antibody plus rIL-4. Lymphocytes in the Peyer's patches (PP) of mice with oral administration of actarit suppressed the production of IgA (not IgM and IgG) by B-cells stimulated with LPS. Actarit affected neither the serum level of IgA nor IgA secretion from the gut of mice without LPS stimulation. Actarit did not change the percentage of Thy-1+ cells in the PP lymphocyte population or that of CD4+ or CD8+ cells in the Thy-1+ fraction of PP lymphocytes. The suppressive effect of PP lymphocytes from mice treated with actarit was abrogated by the elimination of CD4+ cells (not CD8+ cells) from PP lymphocytes. These results suggest that actarit activates CD4+ suppressor T-cells in the PP, resulting in a specific suppression of IgA production after LPS stimulation.
我们研究了新型抗风湿药物阿克他利对小鼠经脂多糖（LPS）刺激后抗体产生的影响。阿克他利不影响经LPS或抗小鼠μ链抗体加重组白细胞介素-4（rIL-4）刺激的B细胞的增殖反应。口服阿克他利的小鼠派尔集合淋巴结（PP）中的淋巴细胞抑制了经LPS刺激的B细胞产生IgA（而非IgM和IgG）。阿克他利既不影响无LPS刺激的小鼠血清IgA水平，也不影响其肠道IgA分泌。阿克他利未改变PP淋巴细胞群体中Thy-1+细胞的百分比，也未改变PP淋巴细胞Thy-1+亚群中CD4+或CD8+细胞的百分比。通过从PP淋巴细胞中去除CD4+细胞（而非CD8+细胞），可消除经阿克他利处理的小鼠PP淋巴细胞的抑制作用。这些结果表明，阿克他利激活了PP中的CD4+抑制性T细胞，导致LPS刺激后IgA产生受到特异性抑制。
