gms | German Medical Science

21. Jahrestagung der Deutschen Gesellschaft für Pädiatrische Infektiologie (DGPI)

Deutsche Gesellschaft für Pädiatrische Infektiologie (DGPI)

25.04. - 27.04.2013, Würzburg

Low number of interferon-gamma-producing varicella-zoster-virus (VZV)-specific T-cells in autoimmune arthritis patients

Meeting Abstract

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  • corresponding author presenting/speaker G. Almanzar - University of Würzburg, Department of Pediatrics - Würzburg, Deutschland
  • I. Sinn - University of Würzburg, Department of Pediatrics - Würzburg, Deutschland
  • K. Höfner - University of Würzburg, Department of Pediatrics - Würzburg, Deutschland
  • M. Prelog - University of Würzburg, Department of Pediatrics - Würzburg, Deutschland

Deutsche Gesellschaft für Pädiatrische Infektiologie. 21. Jahrestagung der Deutschen Gesellschaft für Pädiatrische Infektiologie (DGPI). Würzburg, 25.-27.04.2013. Düsseldorf: German Medical Science GMS Publishing House; 2013. Doc13dgpi49

doi: 10.3205/13dgpi49, urn:nbn:de:0183-13dgpi493

Veröffentlicht: 28. März 2013

© 2013 Almanzar et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Background and aims: Varicella-zoster-virus (VZV) is a herpes virus that establishes a life-long latent infection with risk of reactivation (shingles) particularly in immunosuppressed and patients with autoimmune disorders. This study evaluated the humoral (IgG concentration and avidity) and the cellular immune response to VZV in patients with juvenile idiopathic arthritis (JIA), with rheumatoid arthritis (RA), healthy children (HC) and healthy adults (HA).

Methods: VZV-IgG concentrations (UI/mL) and avidities (relative avidity index:RAI) were determined by ELISA (Euroimmune). VZV-specific interferon-gamma(IFNgamma)-producing T-cells were determined by ELISPOT and expressed as spots forming units (SFU/106cells) in 36JIA, 39RA, 11HC and 28HA.

Results: No differences in the VZV-IgG concentrations (JIA:2732±624,RA:1473±379,HC:2803±950,HA:2315±515UI/mL) or in the avidities (RAI:JIA:79.7±1.7%,RA:77.2±1.9%,HC:77.5±1.7%,HA:77.7±1.3%) were found in all groups. The frequency of IFNgamma-producing VZV-specific T-cells was low. RA showed significantly lower SFU compared to HA (mean±sem,RA:18.6±3.1;CA:63.3±10,p<0.001) and to JIA (JIA:38.2±6.9,p<0.05). No significant differences were determined between JIA and HC (JIA:38.2±6.9;HC:42.3±11.3). The influence of the therapy on the frequency of IFNgamma-producing VZV-specific T-cells in RA and JIA patients was analyzed. RA with non-steroidal anti-inflammatory drugs (NSAID) showed significantly higher SFU than untreated patients (NSAID+:22.1±3.9;NSAID-:12.1±5.4,p<0.05), with similar findings in JIA (NSAID+:51.9±9.2;NSAID-:22.8±9.2,p<0.01). No differences were found in patients treated with glucocorticoids or methotrexate.

Conclusions: These data suggest a reduction of the cellular immune response to VZV in RA. However, NSAID treatment enhanced the number of the IFNgamma-producing VZV-specific T cells in JIA and RA, suggesting patients with less inflammation. The long-term maintenance of anti-VZV cellular immunity in patients with autoimmune conditions and immunosuppressive treatments may need further investigation to prevent VZV reactivation.