Measles: immunosuppression, interleukin-12, and complement receptors.

Abstract

Measles virus, the first pathogen recognized to cause immunosuppression, induces profound and prolonged abnormalities in cellular immune responses in infected hosts. The ability of measles virus to specifically ablate monocyte/macrophage and dendritic cell production of interleukin (IL)-12 provides a potentially unifying mechanism for many of these in vivo and in vitro abnormalities. Cross-linking of the cellular receptor for measles virus, the complement regulatory protein CD46, is sufficient to inhibit IL-12 production. CD46-mediated downregulation of IL-12 has turned out to be a specific instance of a more general pattern of tight inhibitory control over IL-12 production effected by complement and phagocytic receptors on antigen-presenting cells. Exploitation of these pathways by other intracellular pathogens is likely.