KLRK1 and hepatitis A virus infection: Our results could not be interpreted as result of a developmental and/or functional defect of iNKT cells in the absence of NKG2D as experiments performed with anti-NKG2D neutralizing antibodies showed a reduced activation of iNKT cells and a resistance of Con A-induced hepatitis similar to the one observed in genetically modified Klrk1−/− mice.