| B7RP-1 blockade ameliorates autoimmunity through regulation of follicular helper T cells. | |
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MedLine Citation:
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PMID: 19155489 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Autoimmune diseases are marked by the presence of class-switched, high-affinity autoantibodies with pathogenic potential. Costimulation plays an important role in the activation of T cells and the development of T cell-dependent B cell responses. ICOS plays an indispensable role in the development of follicular helper T cells (T(FH) cells), which provide cognate help to germinal center (GC) B cells. We show that the levels of T(FH) cells and GC B cells in two different models of autoimmunity, the New Zealand Black/New Zealand White (NZB/NZW) F(1) mouse model of systemic lupus erythematosus and the collagen-induced arthritis model of rheumatoid arthritis, are dependent on the maintenance of the ICOS/B7RP-1 pathway. Treatment with an anti-B7RP-1 Ab ameliorates disease manifestations and leads to a decrease in T(FH) cells and GC B cells as well as an overall decrease in the frequency of ICOS(+) T cells. Coculture experiments of Ag-primed B cells with CXCR5(+) or CXCR5(-) T cells show that blocking B7RP-1 does not directly impact the production of IgG by B cells. These findings further support the role of ICOS in autoimmunity and suggest that the expansion of the T(FH) cell pool is an important mechanism by which ICOS regulates Ab production. |
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Authors:
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Yi-Ling Hu; Daniela P Metz; James Chung; Gerald Siu; Ming Zhang |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 182 ISSN: 1550-6606 ISO Abbreviation: J. Immunol. Publication Date: 2009 Feb |
Date Detail:
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Created Date: 2009-01-21 Completed Date: 2009-03-30 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 1421-8 Citation Subset: AIM; IM |
Affiliation:
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Department of Inflammation, Amgen, Inc., Thousand Oaks, CA 91320, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antibodies, Blocking / administration & dosage* Antibodies, Monoclonal / administration & dosage* Antigens, CD80 / immunology*, physiology Antigens, Differentiation, T-Lymphocyte / immunology, physiology Arthritis, Experimental / immunology, pathology, therapy Autoantibodies / biosynthesis*, metabolism B-Lymphocytes / immunology, metabolism, pathology Cell Differentiation / immunology* Female Germinal Center / immunology*, metabolism, pathology Lupus Erythematosus, Systemic / immunology, pathology, therapy Lymphocyte Activation / immunology Male Mice Mice, Inbred BALB C Mice, Inbred DBA Mice, Inbred NZB Random Allocation Signal Transduction / immunology* T-Lymphocytes, Helper-Inducer / immunology*, metabolism, pathology |
| Chemical | |
Reg. No./Substance:
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0/Antibodies, Blocking; 0/Antibodies, Monoclonal; 0/Antigens, CD80; 0/Antigens, Differentiation, T-Lymphocyte; 0/Autoantibodies; 0/B7-related protein-1; 0/inducible T-cell co-stimulator |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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