Mincle signaling in the innate immune response after traumatic brain injury

Juan Pablo De Rivero Vaccari, Juan Carlos De Rivero Vaccari, Frank J. Brand, Aldo F. Berti, Ofelia F. Alonso, M. Ross Bullock

Research output: Contribution to journalArticlepeer-review

40 Scopus citations


The innate immune response contributes to the inflammatory activity after traumatic brain injury (TBI). In the present study we identify macrophage-inducible C-type lectin (mincle) as a pattern recognition receptor that contributes to innate immunity in neurons after TBI. Here we report that mincle is activated by SAP130 in cortical neurons in culture, resulting in production of the inflammatory cytokine TNF. In addition, mincle and SAP130 are elevated in the brain and cerebrospinal fluid of humans after TBI and the brain of rodents after fluid percussion brain injury. Thus, these findings suggest the involvement of mincle to the pathology of TBI. Importantly, blocking mincle with a neutralizing antibody against mincle in cortical neurons in culture treated with SAP130 resulted in inhibition of mincle signaling and decreased TNF production. Therefore, our findings identify mincle as a contributor to the inflammatory response after TBI.

Original languageEnglish (US)
Pages (from-to)228-236
Number of pages9
JournalJournal of neurotrauma
Issue number4
StatePublished - Feb 15 2015


  • innate immunity
  • mincle
  • neuroinflammation
  • neurons
  • traumatic brain injury

ASJC Scopus subject areas

  • Clinical Neurology


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