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Infection and Immunity, May 2002, p. 2598-2604, Vol. 70, No. 5
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.5.2598-2604.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Immunoglobulin G Monoclonal Antibodies to Cryptococcus neoformans Protect Mice Deficient in Complement Component C3

Scott Shapiro,1 David O. Beenhouwer,1,2,{dagger} Marta Feldmesser,2 Carlos Taborda,3 Michael C. Carroll,4 Arturo Casadevall,2,3 and Matthew D. Scharff1*

Departments of Cell Biology,1 Medicine,2 Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461,3 Department of Pediatrics and The Center for Blood Research, Harvard Medical School, Boston, Massachusetts 021154

Received 2 October 2001/ Returned for modification 15 November 2001/ Accepted 29 January 2002

Passive administration of monoclonal antibodies (MAbs) to the capsular polysaccharide of Cryptococcus neoformans can alter the course of infection in mice. In a murine model of cryptococcal infection, immunoglobulin G1 (IgG1), IgG2a, and IgG2b switch variants of the anti-capsular 3E5 MAb prolong the survival of lethally infected mice, whereas the 3E5 IgG3 MAb does not protect and in some cases enhances infection, shortening the life spans of infected mice. We examined the role of complement component C3 in Ab-mediated protection by determining the efficacy of the four mouse IgG subclasses against C. neoformans in mice genetically deficient in factor C3 as well as mice acutely depleted of C3. Similar to other complement-deficient animal models, C3-/- mice and mice depleted of C3 by cobra venom factor were more susceptible to C. neoformans infection than control mice, providing further evidence that complement is important in the host defense against the fungus. In the absence of C3, all IgG isotypes prolonged the lives of mice infected with C. neoformans, indicating that protection by IgG does not require the complement pathways. Furthermore, we observed protection with IgG3 in the complement-deficient mice, suggesting that complement is involved in the lack of protection observed with IgG3 in other mouse models.

* Corresponding author. Mailing address: Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461. Phone: (718) 430-3527. Fax: (718) 430-8574. E-mail: scharff{at}aecom.yu.edu.

Editor: T. R. Kozel

{dagger} Present address: Department of Microbiology, Immunology and Molecular Genetics, UCLA, Los Angeles, CA 90025.

Infection and Immunity, May 2002, p. 2598-2604, Vol. 70, No. 5
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.5.2598-2604.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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