McGarry M P, Brandt E J, Swank R T
Am J Pathol. 1976 Dec;85(3):685-92.
Humans with Chediak-Higashi syndrome (CHS) and mice carrying the beige mutation have a heritable defect which results in the presence of giant inclusion granules in the cytoplasm in a wide variety of cells and a markedly increased susceptibility to infections. To test whether this increased susceptibility to infection might be a consequence of impaired accumulation of granulocytes at sites of inflammatory-immune stimulation, we quantitated the exudation of granulocytes into the peritoneum in response to secondary tetanus toxoid challenge in normal mice and in two inbred mouse strains with the beige mutation. Neutrophil and eosinophil granulocyte responses in the peritoneal cavity were not diminished in the beige mice as compared to normal mice when previously sensitized animals were challenged intraperitoneally with tetanus toxoid. Since accumulation of cells at the in vivo site of inflammatory immune stimulation did not seem impaired in the mutant beige mice, it would appear that their increased susceptibility to infections is not due to impairment of cellular exudative responses, including the immune components of the eosinophil response.
患有切-东综合征（CHS）的人类和携带米色突变的小鼠存在一种遗传性缺陷，这导致多种细胞的细胞质中出现巨大的包涵体颗粒，并且对感染的易感性显著增加。为了测试这种对感染易感性的增加是否可能是炎症免疫刺激部位粒细胞积聚受损的结果，我们对正常小鼠以及两种携带米色突变的近交系小鼠在二次破伤风类毒素攻击后，粒细胞向腹膜的渗出情况进行了定量分析。当先前致敏的动物经腹腔注射破伤风类毒素进行攻击时，与正常小鼠相比，米色小鼠腹腔内的中性粒细胞和嗜酸性粒细胞反应并未减弱。由于在突变的米色小鼠中，炎症免疫刺激的体内部位细胞的积聚似乎并未受损，因此它们对感染易感性的增加似乎并非由于包括嗜酸性粒细胞反应的免疫成分在内的细胞渗出反应受损所致。
