Liew F Y, Parkinson C, Millott S, Severn A, Carrier M
Department of Experimental Immunology, Wellcome Biotech, Beckenham, Kent, U.K.
Immunology. 1990 Apr;69(4):570-3.
Genetically resistant CBA mice developed significantly larger lesions to Leishmania major infection when they were injected with rabbit anti-tumour necrosis factor (TNF)-specific antibodies compared to control mice injected with normal rabbit immunoglobulin. BALB/c mice recovered from a previous infection following prophylactic sublethal irradiation also developed exacerbated lesions when treated with the anti-TNF antibody. Injection of TNF into the lesion of infected CBA mice significantly reduced the lesion development. Furthermore, TNF activates macrophages to kill Leishmania in vitro. These data demonstrate that TNF plays an important role in mediating host-protection against cutaneous leishmaniasis.
与注射正常兔免疫球蛋白的对照小鼠相比,当注射兔抗肿瘤坏死因子(TNF)特异性抗体时,基因抗性CBA小鼠在感染硕大利什曼原虫后出现的损伤明显更大。先前经亚致死剂量预防性照射后从感染中恢复的BALB/c小鼠在用抗TNF抗体治疗时也出现了加重的损伤。向感染的CBA小鼠损伤部位注射TNF可显著减少损伤的发展。此外,TNF在体外可激活巨噬细胞以杀死利什曼原虫。这些数据表明,TNF在介导宿主对皮肤利什曼病的保护中起重要作用。