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Report on the 2nd scientific meeting of the "Verein zur F?rderung des Wissenschaftlichen Nachwuchses in der Neurologie" (NEUROWIND e.V.) held in Motzen, Germany, Oct. 29'th - Oct. 31'st, 2010

DOI: 10.1186/2040-7378-3-3

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Abstract:

The technology of two-photon-microscopy even allows monitoring immune cell-target interactions within the CNS parenchyma. In a recently published study, Volker Siffrin from the group of Frauke Zipp investigated the interaction of encephalitogenic CD4+ T cells with neuronal structures in the brain stem in vivo. Interestingly, myelin antigen reactive (2D2) T cells of the Th17 phenotype were able to interact with (and damage) axons. While IFN-γ producing Th1 cells failed to induce neuronal apoptosis, Th17 cells were very efficient in promoting axonal damage. The mechanism of lesion development has not yet been entirely unraveled. While the interaction between CD4+ T cells and axons was independent of the T cell receptor (which in this case was MOG35-55 specific) and thus not restricted by MHC class II expression on axons, ICAM-1 expression by axons and LFA-1 expression by T cells was critically required for Th17-axonal interaction. Axons responded to Th17 cell-mediated attack by Ca2+ influx, which was partially reversible by blockade of NMDA receptors[4]. Thus, Th17 cells exerted effector functions in the CNS that appeared to be unique to this effector T cell subset.In order to test the functional relevance of susceptibility genes identified in the genome-wide association studies in MS, it is a promising approach to investigate whether the expression level of the corresponding gene products on T cells correlates with an altered functional phenotype of these cells. Melanie Piedavent from the group of Manuel Friese analysed the expression of CD226 on human and mouse CD4+ and CD8+ T cells. CD226 interacts with its ligand CD155 on antigen presenting cells and has a role as a costimulatory molecule. The nonsynonymous single nucleotide polymorphism (SNP) rs763361/Gly307Ser in exon 7 of CD226 leads to the substitution of serine for glycine in the amino acid sequence of CD226 and has been associated with increased risk for type 1 diabetes, MS, rheumatoid arthritis and autoimmu

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