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Strathprints serves world leading Open Access research by the University of Strathclyde, including research by the Strathclyde Institute of Pharmacy and Biomedical Sciences (SIPBS), where research centres such as the Industrial Biotechnology Innovation Centre (IBioIC), the Cancer Research UK Formulation Unit, SeaBioTech and the Centre for Biophotonics are based.

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Toxoplasma gondii-specific immunoglobulin M limits parasite dissemination by preventing host cell invasion

Couper, K N and Roberts, C W and Brombacher, F and Alexander, J and Johnson, L L (2005) Toxoplasma gondii-specific immunoglobulin M limits parasite dissemination by preventing host cell invasion. Infection and Immunity, 73 (12). pp. 8060-8068. ISSN 0019-9567

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Abstract

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.