Measles virus infection causes strong immunosuppression. Measles virus wild strains (clinical isolates) recognize CD150/SLAM (signaling lymphocyte activation molecule) as a receptor. However, laboratory (vaccine) strains only recognize CD46. SLAM is strongly expresseed on memory T cells and B cells, but is also expressed on monocytes, T cells, B cells, and matured DCs. SLAM is not expressed on immature DCs, epithelial cells, and endothelial cells. On the other hand, CD46 is expressed on variety of cell types. Infection of SLAM-negative mucosal epithelial cells with measles virus wild strains is thought to be mediated by an as yet unknown "third" receptor [34, 35] . The HA protein of wild virus strain, but not the laboratory strain, induces cytokines such as IL-1α, IL-1β, IL-6, IL-8, and IL-12 via the TLR2 signaling pathway [36] . These cytokines activate and recruit immune cells to the site of inflammation, where the activated immune cells are infected with measles virus via SLAM. The infection and cytokine production are thus propagated.