The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1998/2/641/ $5.00
The Journal of Experimental Medicine, Volume 187, Number 4, February 16, 1998 641-648

Articles

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

RuiRong Yuan*, Raphael Clynes{ddagger}, Jin Oh*, Jeffrey V. Ravetch{ddagger}, and Matthew D. Scharff*

From the * Department of Cell Biology of the Albert Einstein College of Medicine, Bronx, New York, 10461, and the {ddagger} 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 {gamma} chain of FcRs. Passive administration of an IgG1 mAb protects FcR{gamma}+/– mice infected with C. neoformans, but fails to protect FcR{gamma}–/– mice, indicating that the {gamma} chain acting through Fc{gamma}RI 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 {gamma} 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{gamma} chain. In contrast, opsonization of C. neoformans by IgG3 does not require the presence of the {gamma} chain or of FcRII, and the internalization of IgG3-treated organisms does not arrest fungal growth.

This work was supported by a grant (R35 CA-39838) from the National Institutes of Health (NIH) and by the Harry Eagle Chair from the National Women's Division of the Albert Einstein College of Medicine to M.D. Scharff; by a fellowship from the Aaron Diamond Foundation to R. Yuan; and by grants from the NIH to J.V. Ravetch (RO1 AI-35875) and R. Clynes (KO8 DK-02468).

Address correspondence to Matthew D. Scharff, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY, 10461. Phone: 718-430-3504; Fax: 718-430-8574; E-mail: scharff{at}aecom.yu.edu

Note added in proof: While this paper was in press, Gavin et al. reported that Fc{gamma}RI{alpha} bound and mediated phagocytosis of IgG3 SRBCs. Gavin, A.L., N. Barnes, H.M. Dijstelbloem, and P.M. Hogarth. 1998. J. Immunol. 160:20–23.

1 Abbreviations used in this paper: ADCC, antibody-dependent cytotoxicity; GXM, glucuronoxylomannan.


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