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  • Brauner, SusannaKarolinska Institutet (author)

H1N1 vaccination in Sjogren's syndrome triggers polyclonal B cell activation and promotes autoantibody production

  • Article/chapterEnglish2017

Publisher, publication year, extent ...

  • 2017-07-31
  • BMJ,2017
  • printrdacarrier

Numbers

  • LIBRIS-ID:oai:DiVA.org:uu-336305
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-336305URI
  • https://doi.org/10.1136/annrheumdis-2016-210509DOI
  • http://kipublications.ki.se/Default.aspx?queryparsed=id:136611321URI

Supplementary language notes

  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

Notes

  • ObjectivesVaccination of patients with rheumatic disease has been reported to result in lower antibody titres than in healthy individuals. However, studies primarily include patients on immunosuppressive therapy. Here, we investigated the immune response of treatment-naive patients diagnosed with primary Sjogren's syndrome (pSS) to an H1N1 influenza vaccine.Methods Patients with Sjogren's syndrome without immunomodulatory treatment and age-matched and gender-matched healthy controls were immunised with an H1N1 influenza vaccine and monitored for serological and cellular immune responses. Clinical symptoms were monitored with a standardised form. IgG class switch and plasma cell differentiation were induced in vitro in purified naive B cells of untreated and hydroxychloroquine-treated patients and healthy controls. Gene expression was assessed by NanoString technology.ResultsSurprisingly, treatment-naive patients with Sjogren's syndrome developed higher H1N1 IgG titres of greater avidity than healthy controls on vaccination. Notably, off-target B cells were also triggered resulting in increased anti-EBV and autoantibody titres. Endosomal toll-like receptor activation of naive B cells in vitro revealed a greater propensity of patient-derived cells to differentiate into plasmablasts and higher production of class switched IgG. The amplified plasma cell differentiation and class switch could be induced in cells from healthy donors by preincubation with type 1 interferon, but was abolished in hydroxychloroquine-treated patients and after in vitro exposure of naive B cells to chloroquine.ConclusionsThis comprehensive analysis of the immune response in autoimmune patients to exogenous stimulation identifies a mechanistic basis for the B cell hyperactivity in Sjogren's syndrome, and suggests that caution is warranted when considering vaccination in non-treated autoimmune patients.

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  • Folkersen, LasseKarolinska Univ Hosptial, Karolinska Inst, Dept Med, Stockholm, Sweden. (author)
  • Kvarnstrom, MarikaKarolinska Institutet (author)
  • Meisgen, SabrinaKarolinska Univ Hosptial, Karolinska Inst, Dept Med, Stockholm, Sweden. (author)
  • Petersen, SvenKarolinska Univ Hosptial, Karolinska Inst, Dept Med, Stockholm, Sweden. (author)
  • Franzen-Malmros, MichaelaKarolinska Univ Hosptial, Karolinska Inst, Dept Med, Stockholm, Sweden. (author)
  • Mofors, JohannesKarolinska Institutet (author)
  • Brokstad, Karl A.Karolinska Institutet (author)
  • Klareskog, LarsKarolinska Institutet (author)
  • Jonsson, RolandUniv Bergen, Dept Clin Sci, Broegelmann Res Lab, Bergen, Norway. (author)
  • Westerberg, Lisa S.Karolinska Institutet (author)
  • Trollmo, ChristinaKarolinska Univ Hosptial, Karolinska Inst, Dept Med, Stockholm, Sweden. (author)
  • Malmstrom, VivianneKarolinska Institutet (author)
  • Ambrosi, AurelieKarolinska Univ Hosptial, Karolinska Inst, Dept Med, Stockholm, Sweden. (author)
  • Kuchroo, Vijay K.Uppsala universitet,Reumatologi,Science for Life Laboratory, SciLifeLab (author)
  • Nordmark, GunnelHarvard Med Sch, Evergrande Ctr Immunol Dis, Boston, MA USA.;Brigham & Womens Hosp, 75 Francis St, Boston, MA 02115 USA. (author)
  • Wahren-Herlenius, MarieKarolinska Institutet (author)
  • Karolinska InstitutetKarolinska Univ Hosptial, Karolinska Inst, Dept Med, Stockholm, Sweden. (creator_code:org_t)

Related titles

  • In:Annals of the Rheumatic Diseases: BMJ76:10, s. 1755-17630003-49671468-2060

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