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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 ...

  • 2018-01-22
  • Hoboken :John Wiley & Sons,2018
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:hh-48392
  • https://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-48392URI
  • https://doi.org/10.1002/art.40354DOI
  • https://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-48896URI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:137507113URI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • Funding agency:Alex and Eva Wallströms FoundationEuropean Union Innovative Medicine InitiativeSwedish Strategic Science FoundationSeventh Framework Programme (FP7)Medicinska Forskningsrådet (MFR)
  • 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 ...)

  • Habir, KatrinKarolinska Institutet (författare)
  • Nandakumar, Kutty Selva,1965-Karolinska Institutet(Swepub:hh)kutnam (författare)
  • Saxena, AmitKarolinska Institutet (författare)
  • Xu, BingzeKarolinska Institutet (författare)
  • Holmdahl, RikardKarolinska Institutet (författare)
  • Malin, StephenKarolinska Institutet (författare)
  • Karolinska InstitutetKarolinska University Hospital, Karolinska Institutet, Stockholm, Sweden (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Arthritis & RheumatologyHoboken : John Wiley & Sons70:2, s. 193-2032326-51912326-5205

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