John Libbey Eurotext

European Cytokine Network

Effects of interleukin 17A (IL-17A) neutralization on murine hepatitis virus (MHV-A59) infection Volume 28, numéro 3, September 2017

Illustrations

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Tableaux

Auteurs
1 Instituto de Química y Fisicoquímica Biológicas (UBA-CONICET), Facultad de Farmacia y Bioquímica, Buenos Aires, Argentina
2 Unit of Experimental Medicine, de Duve Institute, Université Catholique de Louvain, Brussels, Belgium
3 Ludwig Institute for Cancer Research, Brussels Branch, B-1200 Brussels, Belgium
* Correspondence: Lilia A. Retegui. IQUIFIB, Facultad de Farmacia y Bioquímica, Junín 956, 1113 Buenos Aires, Argentina
  • Mots-clés : mouse hepatitis virus, interleukin 17A, interleukin 17F, autoantibodies, IFNγ
  • DOI : 10.1684/ecn.2017.0399
  • Page(s) : 111-9
  • Année de parution : 2017

Mice infected with mouse hepatitis virus A59 (MHV-A59) develop hepatitis and autoantibodies (autoAb) to liver and kidney fumarylacetoacetate hydrolase (FAH), a fact closely related to the release of alarmins such as uric acid and/or high-mobility group box protein 1 (HMGB1). We studied the effect of neutralizing monoclonal antibodies (MAb) against IL-17A in our model of mouse MHV-A59-infection. MAb anti-IL-17F and anti-IFNγ were used to complement the study. Results showed that transaminase levels markedly decreased in MHV-A59-infected mice treated with MAb anti-IL-17A whereas plasmatic Ig concentration sharply increased. Conversely, MAb anti-IL-17F enhanced transaminase liberation and did not affect Ig levels. Serum IFNγ was detected in mice infected with MHV-A59 and its concentration increased after MAb anti-IL-17A administration. Besides, MAb anti-IFNγ greatly augmented transaminase plasmatic levels. IL-17A neutralization did not affect MHV-A59-induction of HMGB1 liberation and slightly augmented plasmatic uric acid concentration. However, mice treated with the MAb failed to produce autoAb to FAH. The above results suggest a reciprocal regulation of Th1 and Th17 cells acting on the different MHV-A59 effects. In addition, it is proposed that IL-17A is involved in alarmins adjuvant effects leading to autoAb expression.