期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 206, 期 9, 页码 2013-2025出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20090667
关键词
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资金
- National Institutes of Health (NIH) [RO1A1026296, RO1A108896, T32AI07363]
- MRC [G0802651] Funding Source: UKRI
- Medical Research Council [G0600698B, G0802651] Funding Source: researchfish
The hypothesis that bystander inflammatory signals promote memory B cell (B-MEM) self-renewal and differentiation in an antigen-independent manner is critically evaluated herein. To comprehensively address this hypothesis, a detailed analysis is presented examining the response profiles of B-2 lineage B220(+)IgG(+) B-MEM toward cognate protein antigen in comparison to bystander inflammatory signals. After in vivo antigen encounter, quiescent B-MEM clonally expand. Surprisingly, proliferating B-MEM do not acquire germinal center (GC) B cell markers before generating daughter B-MEM and differentiating into plasma cells or form structurally identifiable GCs. In striking contrast to cognate antigen, inflammatory stimuli, including Toll-like receptor agonists or bystander T cell activation, fail to induce even low levels of B-MEM proliferation or differentiation in vivo. Under the extreme conditions of adjuvanted protein vaccination or acute viral infection, no detectable bystander proliferation or differentiation of B-MEM occurred. The absence of a B-MEM response to nonspecific inflammatory signals clearly shows that B-MEM proliferation and differentiation is a process tightly controlled by the availability of cognate antigen.
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