期刊
JOURNAL OF IMMUNOLOGY
卷 194, 期 12, 页码 5604-5608出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1500201
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类别
资金
- National Institutes of Health [R01 AI039614, R01 AI103760, R37 AI027998, R01 CA071540]
- Minnesota Masonic Charities
- University of Minnesota Office
CD4(+) germinal center (GC)-T follicular helper (Tfh) cells help B cells become long-lived plasma cells and memory cells. The transcriptional repressor Bcl6 plays a key role in GC-Tfh formation by inhibiting the expression of genes that promote differentiation into other lineages. We determined whether BCOR, a component of a Polycomb repressive complex that interacts with the Bcl6 BTB domain, influences GCTfh differentiation. T cell-targeted BCOR deficiency led to a substantial loss of peptide: MHC class II-specific GC-Tfh cells following Listeria monocytogenes infection and a 2-fold decrease following immunization with a peptide in CFA. The reduction in GC-Tfh cells was associated with diminished plasma cell and GC B cell formation. Thus, T cell-expressed BCOR is critical for optimal GC-Tfh cell differentiation and humoral immunity.
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