B cells are required for the induction of intestinal inflammatory lesions in TCRalpha-deficient mice persistently infected with Cryptosporidium parvum

J Parasitol. 2000 Oct;86(5):1073-7. doi: 10.1645/0022-3395(2000)086[1073:BCARFT]2.0.CO;2.

Abstract

Mice with targeted disruptions in the T-cell receptor alpha gene (TCRalpha-/-) spontaneously develop inflammatory intestinal lesions with extensive B-cell lamina propria infiltrates. Cryptosporidium parvum infection accelerates intestinal lesion formation in TCRalpha-/- mice. In the present study, TCRalpha-/- mice were crossed with JH-/- (B-cell-deficient) mice and challenged with C. parvum to determine if B cells are required for intestinal lesion development. TCRalpha-/- x JH-/- mice challenged with C. parvum, either as neonates or adults, became persistently infected, whereas TCRalpha-/+ x JH-/+ heterozygote control mice cleared the parasite. Cryptosporidium parvum colonization of TCRalpha-/- x JH-/- mice was heaviest in the distal ileum, with fewer parasites detected in the cecum and distal colon. Despite persistent infection, TCRalpha-/- x JH-/- mice did not develop inflammatory or hyperplastic intestinal lesions as detected in C. parvum-infected TCRalpha-/- mice. These findings demonstrate that B cells are a necessary component for the development of inflammatory intestinal lesions of C. parvum-infected TCRalpha-/- mice.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • B-Lymphocytes / immunology*
  • Cattle
  • Crosses, Genetic
  • Cryptosporidiosis / immunology*
  • Cryptosporidiosis / parasitology
  • Cryptosporidiosis / pathology*
  • Cryptosporidium parvum / growth & development
  • Cryptosporidium parvum / immunology*
  • Female
  • Gene Targeting
  • Genes, T-Cell Receptor alpha
  • Inflammation
  • Intestines / immunology
  • Intestines / pathology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Receptors, Antigen, T-Cell, alpha-beta / deficiency
  • Receptors, Antigen, T-Cell, alpha-beta / genetics
  • Receptors, Antigen, T-Cell, alpha-beta / immunology*

Substances

  • Receptors, Antigen, T-Cell, alpha-beta