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Germinal Center B C...
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Dahdah, AlbertKarolinska University Hospital, Karolinska Institutet, Stockholm, Sweden
(författare)
Germinal Center B Cells Are Essential for Collagen-Induced Arthritis
- Artikel/kapitelEngelska2018
Förlag, utgivningsår, omfång ...
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2018-01-22
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Hoboken :John Wiley & Sons,2018
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printrdacarrier
Nummerbeteckningar
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LIBRIS-ID:oai:DiVA.org:hh-48392
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https://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-48392URI
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https://doi.org/10.1002/art.40354DOI
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https://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-48896URI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:137507113URI
Kompletterande språkuppgifter
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Språk:engelska
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Sammanfattning på:engelska
Ingår i deldatabas
Klassifikation
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Ämneskategori:ref swepub-contenttype
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Ämneskategori:art swepub-publicationtype
Anmärkningar
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Funding agency:Alex and Eva Wallströms FoundationEuropean Union Innovative Medicine InitiativeSwedish Strategic Science FoundationSeventh Framework Programme (FP7)Medicinska Forskningsrådet (MFR)
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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.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Habir, KatrinKarolinska Institutet
(författare)
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Nandakumar, Kutty Selva,1965-Karolinska Institutet(Swepub:hh)kutnam
(författare)
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Saxena, AmitKarolinska Institutet
(författare)
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Xu, BingzeKarolinska Institutet
(författare)
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Holmdahl, RikardKarolinska Institutet
(författare)
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Malin, StephenKarolinska Institutet
(författare)
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Karolinska InstitutetKarolinska University Hospital, Karolinska Institutet, Stockholm, Sweden
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Arthritis & RheumatologyHoboken : John Wiley & Sons70:2, s. 193-2032326-51912326-5205
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