Brett S J
Laboratory for Leprosy and Mycobacterial Research, National Institute for Medical Research, London, England.
Cell Immunol. 1987 Dec;110(2):379-90. doi: 10.1016/0008-8749(87)90130-4.
The antigen-specific proliferative response of draining lymph node cells was found to follow a similar pattern in both C57BL and BALB/c mice following subcutaneous infection with Mycobacterium lepraemurium (MLM), although the two strains differed in their ability to control bacterial growth at the site of infection. The proliferative response, which was maximal 1-2 weeks postinfection, was T-cell dependent as it was abrogated with anti-Thy 1.2 + C treatment. The response was also abrogated by pretreatment with anti-Lyt 1.2 + C and slightly reduced by treatment with anti-Lyt 2.2 + C. The decline in T-cell responsiveness, at least from 4 to 8 weeks postinfection, may have been associated with prostaglandin production by inflammatory macrophages, as it was partially restored by addition of indomethacin. Also highly purified T lymphocytes from lymph nodes taken 6-8 weeks postinfection gave a strong antigen-specific proliferative response when reconstituted with optimal numbers of syngeneic antigen-presenting cells from uninfected mice. Proliferation was inhibited by peritoneal macrophages from Corynebacterium parvum-pretreated mice and macrophages from C57BL but not BALB/c mice infected with M. lepraemurium which had been elicited with heat-killed (HK) MLM and thioglycollate. Resident peritoneal macrophages from both C57BL and BALB/c mice infected subcutaneously with M. lepraemurium were slightly more inhibitory than normal macrophages but not as inhibitory as macrophages from C. parvum-pretreated mice. Macrophage-dependent inhibition of T-cell proliferation was partially reversed by addition of indomethacin, suggesting these cells were not defective in processing and presentation of HK-MLM antigens, and that the inhibitory effects were associated with prostaglandin production. Resident peritoneal macrophages from both C57BL and BALB/c mice infected subcutaneously with M. lepraemurium produced comparable or slightly elevated levels of IL-1 on stimulation with LPS or HK-MLM.
在感染鼠麻风杆菌（MLM）后，尽管C57BL和BALB/c小鼠在控制感染部位细菌生长的能力上有所不同，但发现引流淋巴结细胞的抗原特异性增殖反应在这两种小鼠中遵循相似的模式。感染后1 - 2周增殖反应达到最大值，该反应依赖于T细胞，因为用抗Thy 1.2 + C处理可消除该反应。用抗Lyt 1.2 + C预处理也可消除该反应，而用抗Lyt 2.2 + C处理则使其略有降低。感染后至少4至8周T细胞反应性的下降可能与炎性巨噬细胞产生前列腺素有关，因为添加消炎痛可部分恢复该反应。同样，感染后6 - 8周取自淋巴结的高度纯化的T淋巴细胞，在用来自未感染小鼠的最佳数量的同基因抗原呈递细胞重构时，会产生强烈的抗原特异性增殖反应。来自经短小棒状杆菌预处理小鼠的腹腔巨噬细胞以及来自感染了热灭活（HK）MLM和巯基乙酸盐的鼠麻风杆菌的C57BL小鼠而非BALB/c小鼠的巨噬细胞可抑制增殖。皮下感染鼠麻风杆菌的C57BL和BALB/c小鼠的常驻腹腔巨噬细胞比正常巨噬细胞的抑制作用略强，但不如经短小棒状杆菌预处理小鼠的巨噬细胞的抑制作用强。添加消炎痛可部分逆转巨噬细胞依赖性的T细胞增殖抑制，这表明这些细胞在处理和呈递HK - MLM抗原方面没有缺陷，并且抑制作用与前列腺素的产生有关。皮下感染鼠麻风杆菌的C57BL和BALB/c小鼠的常驻腹腔巨噬细胞在用LPS或HK - MLM刺激时产生相当或略高的IL - 1水平。
