Even if type I NKT expand during various types of infections [16], it was found that the activation of type I NKT by microbial antigens seems to be due at least to two different mechanisms: (i) direct binding of microbial antigens to TCR of type I NKT (direct recognition [19,20]); (ii) type I NKT expansion mediated by cytokines (IL12-IL18) released by other cells (antigen presenting cells like dendritic cells, NK, T cells) during infections (indirect recognition [21,22]). This evidence concerns the gene IL18 and infection.