{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T10:28:47Z","timestamp":1770719327228,"version":"3.49.0"},"reference-count":33,"publisher":"Rockefeller University Press","issue":"4","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1998,2,16]]},"abstract":"<jats:p>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 \u03b3 chain of FcRs. Passive administration of an IgG1 mAb protects FcR\u03b3+\/\u2212 mice infected with C. neoformans, but fails to protect FcR\u03b3\u2212\/\u2212 mice, indicating that the \u03b3 chain acting through Fc\u03b3RI 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 \u03b3 chain\u2013deficient 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\u03b3 chain. In contrast, opsonization of C. neoformans by IgG3 does not require the presence of the \u03b3 chain or of FcRII, and the internalization of IgG3-treated organisms does not arrest fungal growth.<\/jats:p>","DOI":"10.1084\/jem.187.4.641","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:49:30Z","timestamp":1027702170000},"page":"641-648","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":64,"title":["Antibody-mediated Modulation of <i>Cryptococcus neoformans<\/i> Infection Is Dependent on Distinct Fc Receptor Functions and IgG Subclasses"],"prefix":"10.1084","volume":"187","author":[{"given":"RuiRong","family":"Yuan","sequence":"first","affiliation":[{"name":"From the *Department of Cell Biology of the Albert Einstein College of Medicine, Bronx, New York, 10461, and the \u2021Lab of Molecular Genetics and Immunology, The Rockefeller University, New York 10021"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Raphael","family":"Clynes","sequence":"additional","affiliation":[{"name":"From the *Department of Cell Biology of the Albert Einstein College of Medicine, Bronx, New York, 10461, and the \u2021Lab of Molecular Genetics and Immunology, The Rockefeller University, New York 10021"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jin","family":"Oh","sequence":"additional","affiliation":[{"name":"From the *Department of Cell Biology of the Albert Einstein College of Medicine, Bronx, New York, 10461, and the \u2021Lab of Molecular Genetics and Immunology, The Rockefeller University, New York 10021"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffrey V.","family":"Ravetch","sequence":"additional","affiliation":[{"name":"From the *Department of Cell Biology of the Albert Einstein College of Medicine, Bronx, New York, 10461, and the \u2021Lab of Molecular Genetics and Immunology, The Rockefeller University, New York 10021"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Matthew D.","family":"Scharff","sequence":"additional","affiliation":[{"name":"From the *Department of Cell Biology of the Albert Einstein College of Medicine, Bronx, New York, 10461, and the \u2021Lab of Molecular Genetics and Immunology, The Rockefeller University, New York 10021"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"291","published-online":{"date-parts":[[1998,2,16]]},"reference":[{"key":"2023072915241199500_B1","doi-asserted-by":"crossref","first-page":"234","DOI":"10.7326\/0003-4819-104-2-234","article-title":"Cryptococcal disease in patients with the acquired immunodeficiency syndrome. 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