Abstract
B cell-deficient C57B1/6 (microMT) mice were resistant to Leishmania major after both primary and secondary parasite challenge. However, unlike in wild-type mice, secondary infection in microMT mice was not accompanied by a marked delayed type hypersensitivity-like response, and interferon-gamma (IFN-gamma) levels were approximately half of those in wild-type mice. These results suggest that B cells are involved in IFN-gamma production and the pathology of secondary infection.
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