Antibody-mediated modulation of Cryptococcus neoformans infection is dependent on distinct Fc receptor functions and IgC subclasses

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

Research output: Contribution to journalArticle

68 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)641-648
Number of pages8
JournalJournal of Experimental Medicine
Volume187
Issue number4
DOIs
StatePublished - Feb 16 1998

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Cryptococcus neoformans
Fc Receptors
Immunoglobulin G
Antibodies
Infection
Growth
Phagocytosis
Antibody Formation
Virulence
Vaccination
Macrophages

ASJC Scopus subject areas

  • Immunology

Cite this

Antibody-mediated modulation of Cryptococcus neoformans infection is dependent on distinct Fc receptor functions and IgC subclasses. / Yuan, RuiRong; Clynes, Raphael; Oh, Jin; Ravetch, Jeffrey V.; Scharff, Matthew D.

In: Journal of Experimental Medicine, Vol. 187, No. 4, 16.02.1998, p. 641-648.

Research output: Contribution to journalArticle

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