Interleukin-2 as a neuromodulator possibly implicated in the physiopathology of sudden infant death syndrome

Neurosci Lett. 2010 Aug 16;480(2):122-6. doi: 10.1016/j.neulet.2010.06.021. Epub 2010 Jun 11.


Dysfunction in vital brainstem centers, including those controlling cardiorespiratory- and sleep/arousal pathophysiology, is reported in sudden infant death syndrome (SIDS). Biological mechanisms underlying SIDS, however, remain unclear. Cytokines are inter-cellular signaling chemicals. They can interact with neurotransmitters and might thus modify neural and neuroimmune functions. Cytokines could therefore act as neuromodulators. Interleukin (IL)-2 is a major immune-related cytokine. It has not been previously depicted in vital brainstem centers. We detected intense neuronal IL-2 immune-reactivity in the SIDS brainstem, namely in vital neural centers. This IL-2 overexpression might interfere with neurotransmitters in those critical brainstem centers, causing disturbed homeostatic control of cardiorespiratory and arousal responses, possibly leading to SIDS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Brain Stem / metabolism*
  • Brain Stem / pathology
  • Female
  • Humans
  • Infant
  • Interleukin-2 / metabolism*
  • Male
  • Neuroimmunomodulation*
  • Sudden Infant Death / immunology*
  • Sudden Infant Death / pathology


  • Interleukin-2