Yamazaki M, Yasui K, Kawai H, Miyagawa Y, Komiyama A, Akabane T
Am J Dis Child. 1984 Feb;138(2):192-6. doi: 10.1001/archpedi.1984.02140400074018.
Immunologic studies were performed on siblings (a 9-year-old boy and an 11-year-old girl) with chronic candidiasis since infancy and showed defective monocyte functions. In vivo migration and in vitro mobility of the monocytes were impaired. In addition, they had defective phagocytosis-killing ability against Candida albicans. There was no factor(s) to inhibit the monocyte functions in the patients' serum, and their mononuclear cells (75% to 80% lymphocytes) did not secrete such an inhibitory factor(s) in vitro. The serum IgG, IgA, IgM, and C3 levels were normal. Delayed hypersensitivity responses to five antigens, including Candida antigen, were absent in the two patients. In vitro T-lymphocyte functions, such as Candida antigen- or mitogen-induced blastogenesis and lymphokine (leukocyte migration inhibitory factor and leukocyte-derived chemotactic factor) production, were normal. The clinical features of our patients were similar to those with chronic mucocutaneous candidiasis (CMC); however, their primary immunologic defect was, unlike that of CMC, in monocytes, but not in T lymphocytes. These results demonstrated a monocyte disorder with defective mobility and phagocytosis-killing ability that contributed to chronic candidiasis.
对自婴儿期起就患有慢性念珠菌病的一对姐弟（一名9岁男孩和一名11岁女孩）进行了免疫学研究，结果显示单核细胞功能存在缺陷。单核细胞的体内迁移和体外运动能力受损。此外，他们对白色念珠菌的吞噬杀伤能力存在缺陷。患者血清中不存在抑制单核细胞功能的因子，并且他们的单核细胞（75%至80%为淋巴细胞）在体外不分泌此类抑制因子。血清IgG、IgA、IgM和C3水平正常。这两名患者对包括念珠菌抗原在内的五种抗原均无迟发型超敏反应。体外T淋巴细胞功能，如念珠菌抗原或丝裂原诱导的细胞增殖和淋巴因子（白细胞迁移抑制因子和白细胞衍生趋化因子）产生，均正常。我们患者的临床特征与慢性黏膜皮肤念珠菌病（CMC）患者相似；然而，与CMC不同的是，他们主要的免疫缺陷在于单核细胞，而非T淋巴细胞。这些结果表明存在一种单核细胞疾病，其迁移和吞噬杀伤能力存在缺陷，这导致了慢性念珠菌病。
