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目的 探讨抗白介素 12 (IL 12 )单克隆抗体治疗实验性慢性结肠炎的机制。方法 用严重联合免疫缺陷 (SCID)小鼠 ,植入同基因源性CD4 5RBhighCD+4 T细胞 ,诱导慢性结肠炎 ,并进行抗IL 12单克隆抗体治疗和观察IL 12在慢性结肠炎中的病理生理作用。结果 在T细胞植入 4周后结肠组织内IL 12P4 0 mRNA含量明显升高 ,抗IL 12单克隆抗体有效地阻断了慢性结肠炎的发生 ,降低了结肠粘膜内CD4 +T细胞和巨噬细胞浸润 ,并抑制肠粘膜内固有层CD4 +T细胞分泌IL 2和IFN γ。结论 IL 12参与了慢性实验性结肠炎的病理生理过程 ,阻断IL 2对治疗慢性结肠炎有效
Objective To investigate the mechanism of anti-interleukin 12 (IL 12) monoclonal antibody in experimental chronic colitis. Methods Severe combined immunodeficiency (SCID) mice were implanted with syngeneic CD4 5RBhighCD + 4 T cells to induce chronic colitis and treated with anti-IL 12 monoclonal antibody and to observe the pathology of IL 12 in chronic colitis Physiological role. Results The level of IL 12P 4 0 mRNA in colon tissues increased significantly after T cells were implanted for 4 weeks. Anti-IL 12 monoclonal antibody effectively blocked the occurrence of chronic colitis and decreased the numbers of CD4 + T cells and macrophages in colonic mucosa Cell infiltration, and inhibit lamina propria CD4 + T cells secreting IL 2 and IFN γ. Conclusion IL 12 participates in the pathophysiological process of chronic experimental colitis, blocking IL 2 is effective in treating chronic colitis