Sonnenfeld G, Salvin S B, Youngner J S
Infect Immun. 1977 Nov;18(2):283-90. doi: 10.1128/iai.18.2.283-290.1977.
The cellular origins of type I and type II interferons released into the circulation of mice with delayed hypersensitivity were investigated. We determined the effect of treatment with various immunosuppressive agents, including cyclophosphamide, cycloheximide, antithymocyte serum, and whole-body X-irradiation, on the release of interferons after intravenous injection of specific (old tuberculin) or nonspecific (lipopolysaccharide) stimuli. The results suggest that (i) a heterogeneous population of lymphocytes (T and B cells) produces type II interferon, (ii) type I interferon is produced by a different cell population, and (iii) type II interferon is produced de novo after challenge with old tuberculin of mice sensitized with Mycobacterium bovis BCG.
对迟发型超敏反应小鼠循环系统中释放的I型和II型干扰素的细胞起源进行了研究。我们测定了用各种免疫抑制剂(包括环磷酰胺、放线菌酮、抗胸腺细胞血清和全身X射线照射)处理后,静脉注射特异性(旧结核菌素)或非特异性(脂多糖)刺激物后干扰素的释放情况。结果表明:(i)淋巴细胞(T细胞和B细胞)的异质性群体产生II型干扰素;(ii)I型干扰素由不同的细胞群体产生;(iii)用卡介苗致敏的小鼠经旧结核菌素攻击后,会重新产生II型干扰素。