期刊
JOURNAL OF IMMUNOLOGY
卷 185, 期 1, 页码 313-326出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0904023
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资金
- National Institutes of Health (National Institute of Arthritis and Musculoskeletal and Skin Diseases) [R01 AR40072, R01 AR44076, P30 AR053495]
- Rheuminations, Inc.
- Arthritis Foundation
- Connecticut Chapter of the Lupus Foundation of America
- La Jolla Institute for Allergy and Immunology
- National Institutes of Health (National Institute of Allergy and Infectious Diseases) [R01 AI072543, R01 AI063107]
- Pew Scholar Award
- Cancer Research Institute Award
Follicular helper T (T-FH) cells, defined by expression of the surface markers CXCR5 and programmed death receptor-1 (PD-1) and synthesis of IL-21, require upregulation of the transcriptional repressor Bcl6 for their development and function in B cell maturation in germinal centers. We have explored the role of B cells and the cytokines IL-6 and IL-21 in the in vivo regulation of Bcl6 expression and T-FH cell development. We found that T-FH cells are characterized by a Bcl6-dependent downregulation of P-selectin glycoprotein ligand 1 (PSGL1, a CCL19-and CCL21-binding protein), indicating that, like CXCR5 and PD-1 upregulation, modulation of PSGL1 expression is part of the T-FH cell program of differentiation. B cells were neither required for initial upregulation of Bcl6 nor PSGL1 downregulation, suggesting these events preceded T-B cell interactions, although they were required for full development of the T-FH cell phenotype, including CXCR5 and PD-1 upregulation, and IL-21 synthesis. Bcl6 upregulation and T-FH cell differentiation were independent of IL-6 and IL-21, revealing that either cytokine is not absolutely required for development of Bcl6 + T-FH cells in vivo. These data increase our understanding of Bcl6 regulation in T-FH cells and their differentiation in vivo and identifies a new surface marker that may be functionally relevant in this subset. The Journal of Immunology, 2010, 185: 313-326.
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