期刊
IMMUNITY
卷 22, 期 6, 页码 749-761出版社
CELL PRESS
DOI: 10.1016/j.immuni.2005.04.012
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资金
- NIAID NIH HHS [T32 AI007051, AI42265] Funding Source: Medline
- NIAMS NIH HHS [AR74315] Funding Source: Medline
Mice with mutations in CD19 Y482/Y513 form germinal centers (GC) but fail to produce high-affinity antibodies. In these mice, GC B cell differentiation, proliferation, and class switching occur but are defective. Altered CD19 signaling results in retention of early GC B cells and reduced proliferation in the follicular dendritic cell (FDC) zone of GC, and causes failure to select for high-affinity mutations. In normal mice, the earliest detectable aggregates of GC B cells are in contact with FDC and IgM(+) cells are only found in the FDC zone, further evidence that the FDC zone is the site of initial GC B cell proliferation, differentiation, and class switching. Proliferation in the non-FDC zone and somatic mutation are not dependent on CD19, indicating separate signaling requirements for the two GC compartments, but these CD19-independent GC functions are not sufficient to generate high-affinity antibodies and B cell memory.
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