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

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