Garside P, Mowat A M
Department of Immunology, Western Infirmary, University of Glasgow.
Immunology. 1993 Feb;78(2):335-7.
We have shown previously that normal mice given interferon-alpha/beta (IFN-alpha/beta) or tumour necrosis factor-alpha (TNF-alpha) develop marked intestinal pathology which is similar to that found in enteropathies associated with cell-mediated immunity in vivo, such as graft-versus-host reaction (GVHR). The enteropathy induced by IFN-alpha/beta and GVHR are both dependent on the presence of natural killer (NK) cells and here we have examined whether NK cells are also required for enteropathy caused by TNF-alpha. Mice injected with recombinant TNF-alpha displayed enhanced splenic NK cell activity and developed significant villus atrophy and crypt hypertrophy in the small intestine. Administration of anti-asialo GM1 antibody abolished the NK cell activity in both normal and TNF-alpha-injected mice, but had no effect on the enteropathy caused by TNF-alpha. We conclude that NK cells are not required for TNF-alpha to damage the small intestine.
我们之前已经表明，给予干扰素-α/β（IFN-α/β）或肿瘤坏死因子-α（TNF-α）的正常小鼠会出现明显的肠道病变，这与体内与细胞介导免疫相关的肠病中发现的病变相似，例如移植物抗宿主反应（GVHR）。IFN-α/β诱导的肠病和GVHR都依赖于自然杀伤（NK）细胞的存在，在此我们研究了TNF-α引起的肠病是否也需要NK细胞。注射重组TNF-α的小鼠脾脏NK细胞活性增强，并在小肠中出现明显的绒毛萎缩和隐窝肥大。给予抗去唾液酸GM1抗体消除了正常小鼠和注射TNF-α小鼠的NK细胞活性，但对TNF-α引起的肠病没有影响。我们得出结论，TNF-α损伤小肠不需要NK细胞。
