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

Yuan, RuiRong; Clynes, Raphael; Oh, Jin; Ravetch, Jeffrey V.; Scharff, Matthew D.

doi:10.1084/jem.187.4.641

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Article| February 16 1998

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

RuiRong Yuan,

RuiRong Yuan

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

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Raphael Clynes,

Raphael Clynes

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

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Jin Oh,

Jin Oh

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

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Jeffrey V. Ravetch,

Jeffrey V. Ravetch

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

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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

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Author and Article Information

RuiRong Yuan

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

Raphael Clynes

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

Jin Oh

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

Jeffrey V. Ravetch

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

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

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: [email protected]

Note added in proof: While this paper was in press, Gavin et al. reported that FcγRIα 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.

Received: November 26 1997

Revision Received: December 16 1997

Online ISSN: 1540-9538

Print ISSN: 0022-1007

1998

J Exp Med (1998) 187 (4): 641–648.

https://doi.org/10.1084/jem.187.4.641

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 γ chain of FcRs. Passive administration of an IgG1 mAb protects FcRγ^+/− mice infected with C. neoformans, but fails to protect FcRγ^−/− mice, indicating that the γ chain acting through FcγRI 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 γ 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 FcRγ chain. In contrast, opsonization of C. neoformans by IgG3 does not require the presence of the γ chain or of FcRII, and the internalization of IgG3-treated organisms does not arrest fungal growth.

1998

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