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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003885naa a2200457 4500
001oai:DiVA.org:hh-48392
003SwePub
008221012s2018 | |||||||||||000 ||eng|
009oai:DiVA.org:hh-48896
009oai:prod.swepub.kib.ki.se:137507113
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-483922 URI
0247 a https://doi.org/10.1002/art.403542 DOI
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-488962 URI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1375071132 URI
040 a (SwePub)hhd (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Dahdah, Albertu Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden4 aut
2451 0a Germinal Center B Cells Are Essential for Collagen-Induced Arthritis
264 c 2018-01-22
264 1a Hoboken :b John Wiley & Sons,c 2018
338 a print2 rdacarrier
500 a Funding agency:Alex and Eva Wallströms FoundationEuropean Union Innovative Medicine InitiativeSwedish Strategic Science FoundationSeventh Framework Programme (FP7)Medicinska Forskningsrådet (MFR)
520 a OBJECTIVE: Rheumatoid arthritis (RA) is considered to be a prototypical autoimmune disorder. Several mechanisms have been proposed for the known pathologic function of B cells in RA, including antigen presentation, cytokine secretion, and humoral immunity. The aim of this study was to address the function of B lymphocytes in experimental arthritis.METHODS: We mapped the adaptive immune response following collagen-induced arthritis (CIA). We subsequently monitored these responses and disease outcomes in genetically modified mouse strains that lack mature B cell or germinal center (GC) functionality in a B cell-intrinsic manner.RESULTS: Following primary immunization, the draining lymph nodes broadly reacted against type II collagen (CII) with the formation of GCs and T cell activation. Mice that lacked mature B cell function were fully protected against CIA and had a severely attenuated ability to mount isotype-switched humoral immune responses against CII. Almost identical results were observed in mice that were selectively deficient in GC responses. Importantly, GC-deficient mice were fully susceptible to collagen antibody-induced arthritis.CONCLUSION: We identified GC formation and anticollagen antibody production as the key pathogenic functions of B cells in CIA. The role of B cells in RA is likely to be more complex. However, targeting the GC reaction could allow for therapeutic interventions that are more refined than general B cell depletion.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Reumatologi och inflammation0 (SwePub)302102 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Rheumatology and Autoimmunity0 (SwePub)302102 hsv//eng
7001 a Habir, Katrinu Karolinska Institutet4 aut
7001 a Nandakumar, Kutty Selva,d 1965-u Karolinska Institutet4 aut0 (Swepub:hh)kutnam
7001 a Saxena, Amitu Karolinska Institutet4 aut
7001 a Xu, Bingzeu Karolinska Institutet4 aut
7001 a Holmdahl, Rikardu Karolinska Institutet4 aut
7001 a Malin, Stephenu Karolinska Institutet4 aut
7102 a Karolinska Institutetb Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden4 org
7730 t Arthritis & Rheumatologyd Hoboken : John Wiley & Sonsg 70:2, s. 193-203q 70:2<193-203x 2326-5191x 2326-5205
8564 u https://doi.org/10.1002/art.40354y Fulltext
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-48392
8564 8u https://doi.org/10.1002/art.40354
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-48896
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:137507113

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