CD4 and infection: In combination with other anti-inflammatory effects of IFNβ such as the inhibition of the differentiation of Th17 cells [45] and the promotion of the differentiation of Tr1 cells [46], the suppression of pro-IL-1β production and inflammasome activation by IFNβ-primed activated CD4+CD45RO+ memory T cells is likely to limit the immune response triggered by infections.