%0 Journal Article
%T Both MHC and non-MHC genes regulate inflammation and T-cell response after traumatic brain injury
%J Brain, behavior, and immunity
%D 2011
%A Al Nimer, Faiez
%A Beyeen, Amennai Daniel
%A Lindblom, Rickard
%A Ström, Mikael
%A Aeinehband, Shahin
%A Lidman, Olle
%A Piehl, Fredrik
%V 25
%N 5
%P 981-990
%X 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-RT1(av1) strain displayed much stronger MHCII (+) presentation, as shown both by immunolabeling and flow cytometry, than the PVG strain, dwarfing the effect of Ciita. The PVG-RT1(av1) strain 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-RT1(av1) strain. 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.<p /> <p>Language: en</p>
%G en
%I Elsevier Publishing
%@ 0889-1591
%U http://dx.doi.org/10.1016/j.bbi.2010.10.017