期刊
JOURNAL OF IMMUNOLOGY
卷 182, 期 4, 页码 1868-1876出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0802501
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资金
- National Institutes of Health [R-01 A1074862, A143603, Al-30048, R-01 A1066232-01, CA038350, A107019]
- Burroughs-Wellcome Fund [1004313]
- Department of Veterans Affairs
- National Multiple Sclerosis Society
- Richard K. Gershon Predoctoral Fellowship
B cells can influence T cell responses by directly presenting Ag or by secreting Ab that binds to Ag to form immunogenic complexes. Conflicting evidence suggests that persisting Ag-Ab complexes propagate long-term T cell memory; yet, other data indicate that memory cells can survive without specific Ag or MHC. In this study, the roles of B cells and Ag-Ab complexes in T cell responses to lymphocytic choriomeningitis virus (LCMV) infection were investigated using B cell-deficient or B cell-competent mice. Despite normal lymphocyte expansion after acute infection, B cell-deficient mice rapidly lost CD4(+) T cell memory, but not CD8(+) T cell memory, during the contraction phase. To determine whether Ag-Ab complexes sustain CD4(+) T cell memory, T cell responses were followed in B cell-transgenic (mIg-Tg) mice that have B cells but neither LCMV-specific Ab nor LCMV-immune complex deposition. In contrast to B cell-deficient mice, mIg-Tg mice retained functional Th cell memory, indicating that B cells selectively preserve CD4(+) T cell memory independently of immune complex formation. An in vivo consequence of losing CD4(+) T cell memory was that B cell-deficient mice were unable to resolve chronic virus infection. These data implicate a B cell function other than Ab production that induces long-term protective immunity. The Journal of Immunology, 2009, 182: 1868-1876.
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