This study showed that LAG3 deficiency leads to a relative skewing of naive CD4 T cells toward a Th1 phenotype, characterized by IFN-γ secretion to control metacestode growth, in mice with chronic infection and in adoptively transferred recipient mice; thus, LAG3 participates in AE disease remission, predominantly mediated by Th1 subset. This evidence concerns the gene CD4 and acrodermatitis enteropathica.