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  • Sjöwall, ChristofferÖstergötlands Läns Landsting,Linköpings universitet,Reumatologi,Hälsouniversitetet,Länskliniken för Reumatologi i Östergötland (author)

Reduced anti-TNFα autoantibody levels coincide with flare in systemic lupus erythematosus

  • Article/chapterEnglish2004

Publisher, publication year, extent ...

  • Elsevier BV,2004
  • printrdacarrier

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  • LIBRIS-ID:oai:DiVA.org:liu-13894
  • https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-13894URI
  • https://doi.org/10.1016/j.jaut.2004.02.003DOI
  • https://lup.lub.lu.se/record/1129777URI

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  • Language:English
  • Summary in:English

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

Notes

  • Deviating cytokine patterns, as a consequence of aberrant immunoregulation, is implicated to be of aetiopathogenetic importance in systemic lupus erythematosus (SLE). To evaluate the possibility of anti-cytokine autoantibody-mediated cytokine regulation/dysregulation, IgG class autoantibodies against cytokines (IL-1β, IL-6, IL-10, TNFα and TGFβ1) were analysed by enzyme-linked immunosorbent assay (ELISA) in serial serum samples from clinically well-characterized SLE patients and in normal human sera (NHS). Anti-TNFα autoantibody levels were lower in patients with active disease compared to inactive disease (P<0.001) as well as to NHS (P<0.001). The anti-TNFα antibody levels correlated inversely to the SLE disease activity index (SLEDAI) (r2=0.07, P<0.01), whereas anti-TGFβ antibodies were raised in SLE and correlated positively to levels of complement factor C1q (r2=0.08, P<0.005). Generally raised anti-cytokine antibody levels and correlations to disease activity measures were found in one individual. Inverse correlations were found comparing SLEDAI scores and autoantibodies to TNFα (r2=0.92) and IL-6 (r2=0.86) and positive correlations were found between levels of anti-TNFα and C1q (r2=0.86) and C3 (r2=0.90). We show, for the first time, a coincidence between reduced anti-TNFα autoantibody levels and disease exacerbation in SLE, which is of interest regarding aetiopathogenesis and disease control.

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  • Ernerudh, JanLinköpings universitet,Klinisk immunologi,Hälsouniversitetet(Swepub:liu)janer15 (author)
  • Bengtsson, AndersLund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Department of Rheumatology, Lund University Hospital, Lund, Sweden(Swepub:lu)reum-abe (author)
  • Sturfelt, GunnarLund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Department of Rheumatology, Lund University Hospital, Lund, Sweden(Swepub:lu)reum-gst (author)
  • Skogh, ThomasÖstergötlands Läns Landsting,Linköpings universitet,Reumatologi,Hälsouniversitetet,Länskliniken för Reumatologi i Östergötland(Swepub:liu)thosk00 (author)
  • Linköpings universitetReumatologi (creator_code:org_t)

Related titles

  • In:Journal of Autoimmunity: Elsevier BV22:4, s. 315-3230896-8411

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