Both MHC and non-MHC genes regulate inflammation and T-cell response after traumatic brain injury

  • Al Nimer F
  • Beyeen A
  • Lindblom R
 et al. 
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Genetic regulation of autoimmune neuroinflammation is a well known phenomenon, but genetic influences on inflammation following traumatic nerve injuries have received little attention. In this study we examined the inflammatory response in a rat traumatic brain injury (TBI) model, with a particular focus on major histocompatibility class II (MHC II) presentation, in two inbred rat strains that have been extensively characterized in experimental autoimmune encephalomyelitis (EAE); DA and PVG. In addition, MHC and Vra4 congenic strains on these backgrounds were studied to give information on MHC and non-MHC gene contribution. Thus, allelic differences in Vra4, harboring the Ciita gene, was found to regulate expression of the invariant chain at the mRNA level, with a much smaller effect exerted by the MHC locus itself. Notably, however, at the protein level the MHC congenic PVG-RT1av1strain displayed much stronger MHCII+presentation, as shown both by immunolabeling and flow cytometry, than the PVG strain, dwarfing the effect of Ciita. The PVG-RT1av1strain had significantly more T-cell influx than both DA and PVG, suggesting regulation both by MHC and non-MHC genes. Finally, in terms of outcome, the EAE susceptible DA strain displayed a significantly smaller resulting lesion volume than the resistant PVG-RT1av1strain. These results provide additional support for a role of adaptive immune response after neurotrauma and demonstrate that outcome is significantly affected by host genetic factors. © 2010 Elsevier Inc.

Author-supplied keywords

  • Ciita
  • Genes
  • Inflammation
  • MHC class II
  • Rat strains
  • T-cells
  • Traumatic brain injury

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  • Faiez Al Nimer

  • Amennai Daniel Beyeen

  • Rickard Lindblom

  • Mikael Ström

  • Shahin Aeinehband

  • Olle Lidman

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