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024 7 |a 10.1016/j.clim.2017.01.015  |2 doi 
028 5 2 |a pubmed25n0895.xml 
035 |a (DE-627)NLM268673519 
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035 |a (PII)S1521-6616(17)30089-X 
040 |a DE-627  |b ger  |c DE-627  |e rakwb 
041 |a eng 
100 1 |a Park, Chanho  |e verfasserin  |4 aut 
245 1 0 |a Positive selection of type II collagen-reactive CD80high marginal zone B cells in DBA/1 mice 
264 1 |c 2017 
336 |a Text  |b txt  |2 rdacontent 
337 |a ƒaComputermedien  |b c  |2 rdamedia 
338 |a ƒa Online-Ressource  |b cr  |2 rdacarrier 
500 |a Date Completed 14.08.2017 
500 |a Date Revised 04.12.2021 
500 |a published: Print-Electronic 
500 |a Citation Status MEDLINE 
520 |a Copyright © 2017 Elsevier Inc. All rights reserved. 
520 |a To investigate whether dysregulated selection of autoreactive marginal zone (MZ) B cells is involved in autoimmune diseases, we examined MZ B cell profile in multiple strains of mice, and found that type II collagen (CII)-reactive autoreactive CD80high MZ B cells spontaneously developed in the DBA/1, but not in C57BL/6 mice. CD80high MZ B cells that were characteristically found in DBA/1 mice expressed higher levels of TACI, SLAM3, and SLAM6 than the usual CD80low MZ B cells. Notably, the CD80high MZ B cells were more sensitive to ibrutinib, a Bruton's tyrosine kinase inhibitor, than CD80low MZ or follicular B cells and their transient depletion via intravenous injection of ibrutinib significantly delayed the induction of collagen-induced arthritis (CIA). In summary, we suggest that the positive selection of CII-reactive CD80high MZ B cells is a critical homeostatic process predisposing the DBA/1 mice to the CIA induction 
650 4 |a Journal Article 
650 4 |a Autoimmunity 
650 4 |a Autoreactive B cell 
650 4 |a CD80 
650 4 |a Collagen-induced arthritis 
650 4 |a DBA/1 mouse 
650 4 |a Marginal zone B cell 
650 7 |a B7-1 Antigen  |2 NLM 
650 7 |a Collagen Type II  |2 NLM 
650 7 |a Ly9 protein, mouse  |2 NLM 
650 7 |a Piperidines  |2 NLM 
650 7 |a Protein Kinase Inhibitors  |2 NLM 
650 7 |a Pyrazoles  |2 NLM 
650 7 |a Pyrimidines  |2 NLM 
650 7 |a Signaling Lymphocytic Activation Molecule Family  |2 NLM 
650 7 |a Slamf6 protein, mouse  |2 NLM 
650 7 |a Tnfrsf13b protein, mouse  |2 NLM 
650 7 |a Transmembrane Activator and CAML Interactor Protein  |2 NLM 
650 7 |a ibrutinib  |2 NLM 
650 7 |a 1X70OSD4VX  |2 NLM 
650 7 |a Protein-Tyrosine Kinases  |2 NLM 
650 7 |a EC 2.7.10.1  |2 NLM 
650 7 |a Agammaglobulinaemia Tyrosine Kinase  |2 NLM 
650 7 |a EC 2.7.10.2  |2 NLM 
650 7 |a Btk protein, mouse  |2 NLM 
650 7 |a EC 2.7.10.2  |2 NLM 
650 7 |a Adenine  |2 NLM 
650 7 |a JAC85A2161  |2 NLM 
700 1 |a Kho, In Seong  |e verfasserin  |4 aut 
700 1 |a In Yang, Jeong  |e verfasserin  |4 aut 
700 1 |a Kim, Min-Jung  |e verfasserin  |4 aut 
700 1 |a Park, Sunhoo  |e verfasserin  |4 aut 
700 1 |a Cha, Hoon-Suk  |e verfasserin  |4 aut 
700 1 |a Lee, Jaejoon  |e verfasserin  |4 aut 
700 1 |a Kim, Tae Jin  |e verfasserin  |4 aut 
773 0 8 |i Enthalten in  |t Clinical immunology (Orlando, Fla.)  |d 1999  |g 178(2017) vom: 28. Mai, Seite 64-73  |w (DE-627)NLM098196855  |x 1521-7035  |7 nnns 
773 1 8 |g volume:178  |g year:2017  |g day:28  |g month:05  |g pages:64-73 
856 4 0 |u http://dx.doi.org/10.1016/j.clim.2017.01.015  |3 Volltext 
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952 |d 178  |j 2017  |b 28  |c 05  |h 64-73