Murray H W, Rubin B Y, Masur H, Roberts R B
N Engl J Med. 1984 Apr 5;310(14):883-9. doi: 10.1056/NEJM198404053101404.
To examine the cellular immune defect that predisposes patients with the acquired immunodeficiency syndrome (AIDS) to opportunistic infections, we tested T lymphocytes from 16 patients for the capacity to secrete macrophage-activating products (lymphokines) including gamma interferon. Mononuclear cells from 10 of 11 patients did not generate an effective lymphokine in response to mitogen, and 11 of 16 produced subnormal levels of gamma interferon (less than 300 U per milliliter). In addition, upon stimulation with specific microbial antigen, cells from none of 14 patients generated active lymphokines, and cells from 13 to 14 completely failed to secrete gamma interferon. However, the antimicrobial function of monocytes from the patients was intact, and once stimulated with normal lymphokines or gamma interferon alone, macrophages derived from patients' monocytes responded with enhanced and effective intracellular antimicrobial activity. These results suggest that impaired lymphokine production may predispose patients with AIDS to opportunistic infections, and they provide a rationale for using gamma interferon as immunotherapy.
为了研究导致获得性免疫缺陷综合征(AIDS)患者易患机会性感染的细胞免疫缺陷,我们检测了16例患者的T淋巴细胞分泌巨噬细胞激活产物(淋巴因子)包括γ干扰素的能力。11例患者中的10例的单核细胞对丝裂原无有效淋巴因子产生,16例中的11例γ干扰素水平低于正常(每毫升低于300 U)。此外,用特异性微生物抗原刺激时,14例患者的细胞均未产生活性淋巴因子,13至14例患者的细胞完全不分泌γ干扰素。然而,患者单核细胞的抗菌功能完好,一旦用正常淋巴因子或单独用γ干扰素刺激,源自患者单核细胞的巨噬细胞会产生增强且有效的细胞内抗菌活性。这些结果提示,淋巴因子产生受损可能使AIDS患者易患机会性感染,并且为使用γ干扰素作为免疫疗法提供了理论依据。