J. Exp. Med., Volume 187, Number 4, February 16, 1998 641-648

Antibody-mediated Modulation of Cryptococcus neoformans Infection Is Dependent on Distinct Fc Receptor Functions and IgG Subclasses

By RuiRong Yuan,^* Raphael Clynes, Jin Oh,^* Jeffrey V. Ravetch, and Matthew D. Scharff^*

From the ^* Department of Cell Biology of the Albert Einstein College of Medicine, Bronx, New York, 10461, and the  Lab of Molecular Genetics and Immunology, The Rockefeller University, New York 10021

Coupling of an antibody response to effector cells through the Fc region of antibodies is a fundamental objective of effective vaccination. We have explored the role of the Fc receptor system in a murine model of Cryptococcus neoformans protection by infecting mice deleted for the common  chain of FcRs. Passive administration of an IgG1 mAb protects FcR^+/ mice infected with C. neoformans, but fails to protect FcR^/ mice, indicating that the  chain acting through FcRI and/or III is essential for IgG1-mediated protection. In contrast, passive administration of an IgG3 mAb with identical specificity resulted in enhanced pathogenicity in  chain-deficient and wild-type mice. In vitro studies with isolated macrophages demonstrate that IgG1-, IgG2a-, and IgG2b-opsonized C. neoformans are not phagocytosed or arrested in their growth in the absence of the FcR chain. In contrast, opsonization of C. neoformans by IgG3 does not require the presence of the  chain or of FcRII, and the internalization of IgG3-treated organisms does not arrest fungal growth.

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