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

K N Couper, C W Roberts, F Brombacher, J Alexander, L L Johnson

Research output: Contribution to journalArticle

33 Citations (Scopus)

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.

LanguageEnglish
Pages8060-8068
Number of pages9
JournalInfection and Immunity
Volume73
Issue number12
DOIs
Publication statusPublished - Dec 2005

Fingerprint

Toxoplasma
Immunoglobulin M
Parasites
Toxoplasmosis
Immunoglobulin Class Switching
Serum
B-Cell Antigen Receptors
Peritoneal Cavity
Interferon-gamma
Immune Sera
B-Lymphocytes
Spleen

Keywords

  • classical complement pathway
  • major surface protein
  • CD8+ T-cells
  • immune-response
  • natural antibodies
  • deficient mice
  • B-cells
  • infection
  • resistance
  • IGM

Cite this

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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.",
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Toxoplasma gondii-specific immunoglobulin M limits parasite dissemination by preventing host cell invasion. / Couper, K N ; Roberts, C W ; Brombacher, F ; Alexander, J ; Johnson, L L .

In: Infection and Immunity, Vol. 73, No. 12, 12.2005, p. 8060-8068.

Research output: Contribution to journalArticle

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