Phagocytosis, chemoluminescence, and intracellular killing of fungi by phagocytes from subjects with deficiency of the second component of complement.

The capacity of phagocytes from animals or humans with complement component deficiency to ingest and kill Candida albicans has been much disputed. We show that peripheral blood polymorphonuclear leukocytes and mononuclear phagocytes from subjects with hereditary C2 deficiency (C2D) ingested C. albicans or Saccharomyces cerevisiae at an abnormally slow rate. After preincubating C. albicans in C2D plasma, the slow rate of phagocytosis was corrected and subsequent intracellular killing of C. Albicans was normal. A normal number of C2D phagocytes reduced nitroblue tetrazolium after stimulation with either phorbol myristate acetate or ingestion of C. albicans. The rate at which chemoluminescence was generated in response to C. albicans was abnormally slow, but peak chemoluminescence produced by C2D phagocytes in response to C. albicans was normal.