+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: not found

      Measles virus-induced immunosuppression: from effectors to mechanisms.

      Medical Microbiology and Immunology
      Antigens, CD, physiology, Cytoskeleton, metabolism, Humans, Immune Evasion, Immune Tolerance, Lymphopenia, immunology, Measles, virology, Measles virus, pathogenicity, Receptors, Cell Surface, Receptors, Virus, T-Lymphocytes

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          Immunosuppression is the major cause of infant death associated with acute measles. Hallmarks of this generalized modulation of immune functions include: (1) lymphopenia, (2) a prolonged cytokine imbalance consistent with suppression of cellular immunity to secondary infections and (3) silencing of peripheral blood lymphocytes that fail to expand in response to ex vivo stimulation. Lymphopenia results from depletion of T cells by mechanisms also involving MV infection, and expression of the major MV receptor CD150 plays an important role for targeting these cells. Virus transfer to T cells is thought to be mediated by dendritic cells (DCs), which are considered as central to the induction of T-cell silencing and functional skewing. MV interaction modulates functional differentiation of DCs, and thereby expression pattern of costimulatory molecules and soluble mediators. Moreover, MV proteins expressed by these cells actively silence T cells by interfering with signaling pathways essential for T-cell activation. As an essential component of this interference, the MV glycoprotein complex activates cellular sphingomyelinases in a contact-dependent manner, and these are effective at preventing stimulated rearrangements of the actin cytoskeleton and thereby morphological and functional polarization and motility of T cells.

          Related collections

          Author and article information


          Comment on this article