T cell development in B cell-deficient mice. IV. The role of B cells as antigen-presenting cells in vivo

B cell-deficient, rabbit anti-mouse IgM-treated mice were compared with normal or normal rabbit immunoglobulin-treated controls in their ability to develop proliferative T cell responses, delayed hypersensitivity, and primary or secondary cytotoxic T cell responses. Immunization with hapten-coupled...

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Published inThe Journal of immunology (1950) Vol. 136; no. 3; pp. 823 - 829
Main Authors Hayglass, KT, Naides, SJ, Scott, CF, Jr, Benacerraf, B, Sy, MS
Format Journal Article
LanguageEnglish
Published Bethesda, MD Am Assoc Immnol 01.02.1986
American Association of Immunologists
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Summary:B cell-deficient, rabbit anti-mouse IgM-treated mice were compared with normal or normal rabbit immunoglobulin-treated controls in their ability to develop proliferative T cell responses, delayed hypersensitivity, and primary or secondary cytotoxic T cell responses. Immunization with hapten-coupled autologous spleen cells resulted in anti-mu-treated mice generating only marginal T cell responses. This decreased responsiveness was shown to be attributable not to an intrinsic T cell defect or to changes in the ability of macrophages from anti-mu-treated mice to present soluble antigen, but rather to the greatly diminished capacity of B cell-deficient spleen cells to present antigen. The results support the concept that B cells play a significant role in antigen presentation required for T cell activation.
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content type line 23
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.136.3.823