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Related Experiment Videos

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

C L Karp1

  • 1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. ckarp@welchlink.welch.jhu.edu

Immunological Reviews
|July 10, 1999
PubMed
Summary

Measles virus causes immune suppression by inhibiting interleukin-12 (IL-12) production in immune cells. This mechanism, mediated by the CD46 receptor, explains many measles-induced immune abnormalities.

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Area of Science:

  • Immunology
  • Virology
  • Cellular Biology

Background:

  • Measles virus is the first identified pathogen causing immunosuppression.
  • It induces significant and lasting defects in cellular immunity.
  • Interleukin-12 (IL-12) is a critical cytokine for cellular immune responses.

Purpose of the Study:

  • To investigate the mechanism by which measles virus causes immunosuppression.
  • To explore the role of IL-12 production in measles-induced immune dysfunction.
  • To identify the cellular receptor involved in measles virus-induced immune modulation.

Main Methods:

  • Studied measles virus infection in host cells.
  • Assessed the production of IL-12 by monocytes, macrophages, and dendritic cells.

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  • Investigated the effect of CD46 receptor cross-linking on IL-12 production.

    • Main Results:

    • Measles virus specifically inhibits IL-12 production by monocytes, macrophages, and dendritic cells.
    • Cross-linking the CD46 receptor, the measles virus cellular receptor, is sufficient to block IL-12 production.
    • This CD46-mediated inhibition of IL-12 is part of a broader inhibitory control mechanism used by complement and phagocytic receptors.

    Conclusions:

    • Measles virus-induced immunosuppression is largely mediated by the downregulation of IL-12 production.
    • The CD46 receptor plays a key role in this inhibitory pathway.
    • Other intracellular pathogens may exploit similar pathways to evade immune responses.