Correspondingly, homozygous Zbtb7bR367Q mutants exhibited significant reductions of thymic and peripheral CD4 T cells, and during infection fewer brain infiltrating proinflammatory leukocytes were observed, confirming the role of CD4 T cell help in promoting ECM pathogenesis (Villegas-Mendez et al., 2012; Ham et al., 2015). This evidence concerns the gene CD4 and infection.