A monocyte disorder in siblings with chronic candidiasis. A combined abnormality of monocyte mobility and phagocytosis-killing ability.

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.