Short report: requirement of b cells for delayed type hypersensitivity-like pathology after secondary infection with Leishmania major in resistant C57BL/6 mice

Abstract

Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2014-09-19T12:34:45Z No. of bitstreams: 1 Dekrey GK Short Report-Requeriment......pdf: 62130 bytes, checksum: 89b0233f4698a99950f720f0f64bbb7f (MD5)Approved for entry into archive by Ana Maria Fiscina Sampaio ([email protected]) on 2014-09-19T12:34:55Z (GMT) No. of bitstreams: 1 Dekrey GK Short Report-Requeriment......pdf: 62130 bytes, checksum: 89b0233f4698a99950f720f0f64bbb7f (MD5)Made available in DSpace on 2014-09-19T12:48:28Z (GMT). No. of bitstreams: 1 Dekrey GK Short Report-Requeriment......pdf: 62130 bytes, checksum: 89b0233f4698a99950f720f0f64bbb7f (MD5) Previous issue date: 2003University of Northern Colorado. Department of Biological Sciences. Greeley, ColoradoColorado State University. Department of Pathology. Fort Collins, ColoradoCentocor, Incorporated, Infectious Diseases. Malvern, PennsylvaniaFundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, BrasilColorado State University. Department of Pathology. Fort Collins, ColoradoB cell-deficient C57Bl/6 ( MT) mice were resistant to Leishmania major after both primary and secondary parasite challenge. However, unlike in wild-type mice, secondary infection in MT mice was not accompanied by a marked delayed type hypersensitivity-like response, and interferon- (IFN- ) levels were approximately half of those in wild-type mice. These results suggest that B cells are involved in IFN- production and the pathology of secondary infection