@Article{ecn.2017.0399,
AUTHOR = {José L. Aparicio, Macarena Ottobre, Maite Duhalde Vega, Jean-Paul Coutelier, Jacques Van Snick, Lilia A. Retegui},
TITLE = {Effects of interleukin 17A (IL-17A) neutralization on murine hepatitis virus (MHV-A59) infection},
JOURNAL = {European Cytokine Network},
VOLUME = {28},
YEAR = {2017},
NUMBER = {3},
PAGES = {111--119},
URL = {http://www.techscience.com/ECN/v28n3/65516},
ISSN = {1952-4005},
ABSTRACT = {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 mouseMHV-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.},
DOI = {10.1684/ecn.2017.0399}
}