Dimitris Papadopoulos

MD, PhD

In our lab we seek to elucidate the mechanisms that underlie disease progression in conditions of inflammatory demyelination, such as multiple sclerosis. To do that we use animal models of immune and chemically-mediated demyelination and human histopathology. 

Keywords: demyelination, inflammation, neurodegeneration, multiple sclerosis, experimental autoimmune encephalomyelitis (EAE)

Selected publications:

1. Tsakiri N, Papadopoulos D, Denis MC, Mitsikostas DD, Kollias G (2012). TNFR2 on non-haematopoietic cells is required for Foxp3+ Treg-cell function and disease suppression in EAE. Eur J Immunol.42(2):403-12.
2. Papadopoulos D, Rundle J, Patel R, Marshall I, Stretton J, Eaton R, Richardson JC, Gonzalez MI, Philpott KL, Reynolds R (2010). FTY720 ameliorates MOG-induced experimental autoimmune encephalomyelitis by suppressing both cellular and humoral immune responses. J Neurosci Res. 88(2):346-59.
3. Papadopoulos D, Dukes S, Patel R, Nicholas R, Vora A, Reynolds R (2009). Substantial archaeocortical atrophy and neuronal loss in multiple sclerosis Brain Pathol 19(2):238-53.