Journal
JOURNAL OF IMMUNOLOGY
Volume 169, Issue 4, Pages 1859-1868Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.169.4.1859
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- NIAID NIH HHS [AI 46806, 5-T32-AI07492] Funding Source: Medline
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The murine low-affinity receptor for IgG, FcgammaRIIB, mediates inhibition of B cell receptor-triggered events in primary B cells. We investigated the expression of FcgammaRIIB on germinal center (GC) cells to better understand its role in memory B cell development. Immunohistological analyses demonstrated differential regulation of FcgammaRIIB on GC cells. Its levels are markedly down-regulated on GC B cells and up-regulated on follicular dendritic cells (FDC) at all times during the GC response. Analyses of surface expression of FcgammaRIIB by flow cytometry and FcgammaRIIB mRNA levels by RT-PCR analysis confirmed that this FcR is down-regulated in GC B cells. In mice lacking FcgammaRIIB, the development of the secondary FDC reticulum in GCs is substantially delayed, although the overall kinetics of the GC response are unaltered. These findings have direct implications for models proposed to account for the selection of high-affinity B cells in the GC and suggest a role for FcgammaRIIB in promoting the maturation of the FDC reticulum.
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