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Mincle signaling in the innate immune response after traumatic brain injury

Juan Carlos de Rivero Vaccari1, Frank J Brand, Aldo F Berti

  • 11 Ophthalmology Department, Louisiana State University School of Medicine/Ochsner Medical Center , New Orleans, Louisiana.

Journal of Neurotrauma
|August 12, 2014
PubMed

Insights

Macrophage-inducible C-type lectin (mincle) acts as a pattern recognition receptor in neurons following traumatic brain injury (TBI). Blocking mincle reduces inflammation and TNF production, suggesting its role in TBI pathology.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Traumatic brain injury (TBI) involves innate immune responses and inflammation.
  • Pattern recognition receptors play a role in the neurological inflammatory activity post-TBI.

Purpose of the Study:

  • To identify pattern recognition receptors involved in neuronal innate immunity after TBI.
  • To investigate the role of macrophage-inducible C-type lectin (mincle) in TBI pathology.

Main Methods:

  • Investigated mincle activation by SAP130 in cultured cortical neurons.
  • Measured TNF production in response to mincle activation.
  • Assessed mincle and SAP130 levels in human and rodent TBI models.
  • Utilized a neutralizing antibody to block mincle activity in vitro.

Main Results:

  • Mincle activation by SAP130 in neurons triggers TNF production.
  • Elevated levels of mincle and SAP130 were observed in human and rodent brains post-TBI.
  • Blocking mincle inhibited mincle signaling and reduced TNF production.

Conclusions:

  • Mincle is a pattern recognition receptor contributing to innate immunity in neurons after TBI.
  • Mincle and SAP130 are implicated in the inflammatory pathology of TBI.
  • Targeting mincle may offer a therapeutic strategy for TBI-related inflammation.
Keywords:
innate immunitymincleneuroinflammationneuronstraumatic brain injury

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