C1q enhances the phagocytosis of Cryptococcus neoformans blastospores by human monocytes

• Published in: The Journal of immunology (1950) Vol. 141; no. 2; pp. 592 - 597
• Main Authors: Bobak, DA, Washburn, RG, Frank, MM
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15.07.1988; American Association of Immunologists
• Subjects: Adjuvants, Immunologic - physiology; Animals; Biological and medical sciences; Blood Physiological Phenomena; Complement Activating Enzymes - physiology; Complement C1 - physiology; Complement C1q; Cryptococcus - immunology; Cryptococcus neoformans; Cryptococcus neoformans - immunology; Drug Contamination; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Humans; Immunobiology; Immunoglobulin G - physiology; Monocytes - immunology; Myeloid cells: ontogeny, maturation, markers, receptors; Opsonin Proteins; Phagocytosis - drug effects; Rabbits; Spores, Fungal - immunology; Fungi; Human; Cryptococcus neoformans; Monocyte; Opsonization; Complement; Fungi Imperfecti; Complement C1q; Phagocytosis; Thallophyta
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.141.2.592

We investigated whether C1q, a subunit of the first component of C, could modulate human peripheral blood monocyte-mediated phagocytosis of Cryptococcus neoformans (CN). Adherence of monocytes to C1q-coated surfaces induced a significant enhancement of ingestion of CN blastospores that had been opsonized with specific anticapsular IgG (IgG-CN). Additionally, C1q enhanced the monocyte-mediated phagocytosis of CN opsonized with C (CN-absorbed, nonimmune, normal human serum; C-CN). Ingestion of IgG- and C-CN by control and C1q-stimulated monocytes was maximal by 1 h of incubation. The monocyte-mediated enhancement of phagocytosis caused by C1q was paralleled by a proportionate increase in fungicidal activity, an effect which was maximal by 3 h of incubation. Human serum albumin-adherent, control monocytes exhibited only a low level of killing after 3 h of incubation. C1q enhancement was blocked by preincubation of the surfaces with a goat, polyclonal F(ab')2 anti-C1q. This study describes a new cellular function for the cell surface C1q receptor: the enhancement of phagocytosis of a pathogenic organism by monocytes.