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Infection and Immunity, December 2005, p. 8060-8068, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8060-8068.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Toxoplasma gondii-Specific Immunoglobulin M Limits Parasite Dissemination by Preventing Host Cell Invasion

Kevin N. Couper,1,2 Craig W. Roberts,1 Frank Brombacher,3 James Alexander,1 and Lawrence L. Johnson2*

Department of Immunology, Strathclyde Institute for Biomedical Sciences, University of Strathclyde, 27 Taylor Street, Glasgow G4 0NR, United Kingdom,1 Trudeau Institute, 154 Algonquin Avenue, Saranac Lake, New York 12983,2 Department of Immunology, University of Cape Town, 7925 Cape Town, South Africa3

Received 18 February 2005/ Returned for modification 2 April 2005/ Accepted 24 August 2005

An important role for immunoglobulin M (IgM) during early acute virulent Toxoplasma gondii infection was identified using IgM–/– mice that lack surface and secretory IgM but maintain normal B-cell functionality and isotype class switching. Following intraperitoneal inoculation with the virulent RH strain, IgM–/– mice displayed significantly fewer peritoneal parasites than wild-type (WT) mice, which correlated with increased tachyzoite dissemination to the liver, lung, and spleen in IgM–/– mice compared with WT mice. Early splenic T-cell activation, as measured by CD69 expression, was augmented in IgM–/– mice, and serum and peritoneal cavity gamma interferon levels were also elevated in IgM–/– mice compared with WT controls. Consequently, the difference in parasite dissemination was not attributable to an impaired proinflammatory immune response in the IgM–/– mice. Specific IgM was found to bind to tachyzoites in vivo in WT mice, and this correlated with an increased ability of antiserum collected from WT mice at day 6 postinfection to block tachyzoite cell invasion, compared with comparable serum collected from IgM–/– mice at the same time point. Tachyzoite invasion of host cells was similar if parasites were incubated with WT or IgM–/– nonimmune serum, suggesting that natural IgM does not function to limit parasite dissemination during early T. gondii infection. Our results highlight an important role for parasite-specific IgM in limiting systemic dissemination of tachyzoites during early acute T. gondii infection.

* Corresponding author. Mailing address: Trudeau Institute, Inc., 154 Algonquin Ave., Saranac Lake, NY 12983. Phone: (518) 891-3080. Fax: (518) 891-5126. E-mail: ljohnson{at}trudeauinstitute.org.

Editor: J. F. Urban, Jr.

Infection and Immunity, December 2005, p. 8060-8068, Vol. 73, No. 12
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.12.8060-8068.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.





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