Kamboj, AmitLu, PingCossoy, Michael BStobart, Jillian LDolhun, Brian AKauppinen, Tiina Mde Murcia, GilbertAnderson, Christopher M2013-05-012013-05-012013-04-22Journal of Neuroinflammation. 2013 Apr 22;10(1):49http://hdl.handle.net/1993/19754Abstract Background Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis characterized by entry of activated T cells and antigen presenting cells into the central nervous system and subsequent autoimmune destruction of nerve myelin. Previous studies revealed that non-selective inhibition of poly(ADP-ribose) polymerases (PARPs) 1 and 2 protect against neuroinflammation and motor dysfunction associated with EAE, but the role of the PARP-2 isoform has not yet been investigated selectively. Results EAE was induced in mice lacking PARP-2, and neurological EAE signs, blood-spine barrier (BSB) permeability, demyelination and inflammatory infiltration were monitored for 35 days after immunization. Mice lacking PARP-2 exhibited significantly reduced overall disease burden and peak neurological dysfunction. PARP-2 deletion also significantly delayed EAE onset and reduced BSB permeability, demyelination and central nervous system (CNS) markers of proinflammatory Th1 and Th17 T helper lymphocytes. Conclusions This study represents the first description of a significant role for PARP-2 in neuroinflammation and neurological dysfunction in EAE.Journal ArticleenAmit Kamboj et al.; licensee BioMed Central Ltd.2013-05-01http://dx.doi.org/10.1186/1742-2094-10-49