Liew F Y, Li Y, Yang D M, Severn A, Cox F E
Wellcome Research Laboratories, Beckenham, Kent, U.K.
Immunology. 1991 Oct;74(2):304-9.
Earlier studies have demonstrated that mice injected subcutaneously or intramuscularly with leishmanial antigens develop significantly exacerbated disease compared with unimmunized controls when challenged with the cutaneous protozoan parasites Leishmania major. We report here that this disease enhancement can be prevented, and protective immunity induced, by the incorporation of recombinant tumour necrosis factor (TNF-alpha) in the immunizing inoculum. This effect of TNF-alpha is dose-dependent and is not evident when TNF-alpha and the antigens are injected into separate sites. Furthermore, TNF-alpha injected together with p183, a peptide known to preferentially stimulate Th2 cells and disease exacerbation in H-2d mice, activates spleen and lymph node cells secreting more interferon-gamma (IFN-gamma) and less interleukin-4 (IL-4) and induces a modest but significant degree of resistance against L. major infection in highly susceptible BALB/c mice.
早期研究表明,与未免疫的对照相比,皮下或肌肉注射利什曼原虫抗原的小鼠在受到皮肤原生动物寄生虫硕大利什曼原虫攻击时,疾病会显著加剧。我们在此报告,通过在免疫接种物中加入重组肿瘤坏死因子(TNF-α),可以预防这种疾病加剧,并诱导保护性免疫。TNF-α的这种作用是剂量依赖性的,当TNF-α和抗原注射到不同部位时则不明显。此外,与已知能优先刺激H-2d小鼠Th2细胞并加剧疾病的p183肽一起注射的TNF-α,可激活分泌更多干扰素-γ(IFN-γ)和更少白细胞介素-4(IL-4)的脾细胞和淋巴结细胞,并在高度易感的BALB/c小鼠中诱导出适度但显著的抗硕大利什曼原虫感染的抵抗力。