Speaker

Reinhard Hohlfeld, Ludwig Maximilians University of Munich, Germany

Reinhard Hohlfeld

Reinhard Hohlfeld is Professor of Neurology and Co-Director of the Institute of Clinical Neuroimmunology, Ludwig Maximilians University of Munich, Germany.
www.klinikum.uni-muenchen.de/Institut-fuer-Klinische-Neuroimmunologie/en/index.html

Hohlfeld research interests include autoimmune mechanisms and pathogenesis of neuroimmunological diseases, especially multiple sclerosis, myasthenia gravis, and inflammatory myopathies. Hohlfeld also has a long-standing interest in mechanisms (and risks) of immunomodulatory therapies.

Hohlfeld is a member of the scientific advisory boards of the German MS Society, International Federation of MS Societies (MSIF), and Progressive MS Alliance (PMSA); member of numerous editorial boards of scientific journals; elected member of the German Academy of Science (Leopoldina); and external scientific member of the Max Planck Society.



Presentation abstract

The T-cell side of multiple sclerosis
Professor Reinhard Hohlfeld MD
Institute of Clinical Neuroimmunology; University Hospital, Ludwig Maximilians University of Munich
Marchioninistr. 15, D-81377 München, Germany
Tel: +49-89-4400-74780 or -74781
Fax: +49-89-4400-74782
E-mail: reinhard.hohlfeld@med.uni-muenchen.de
Email addresses are provided for information in connection with the authors presentation only. Please do not mail credit card information under any circumstances.

T-lymphocytes have long been considered to be crucial players in the pathogenesis of multiple sclerosis (MS) and therefore, prime targets of therapy. Although much has been learned from animal models, There is still a major gap between such models and the human disease. Bridging this gap is a prerequisite for improving the therapy of MS and the aim of our research.

Our basic knowledge of the role of T cells in multiple sclerosis (MS) comes from studies in animal models collectively referred to as experimental autoimmune encephalomyelitis (EAE). EAE can be “transferred” from sick animals into healthy recipient animals by injection of highly purified myelin-autoreactive CD4+ effector T-cells. This observation is a major pillar of our current “CD4-T-cell-centric” view of MS pathogenesis. More recent EAE models, including spontaneous disease models in transgenic mice, generally supports this view. Recent evidence has revealed that CNS autoimmunity might be triggered in the gut-associated lymphoid system by interaction with the intestinal bacterial flora (microbiota). Compared to animal studies on T cells in EAE, research into the role of T cells in human MS faces particular limitations, such as reduced accessibility of biological materials (eg, CNS tissue and CSF), genetic heterogeneity of the human population, and ethical restrictions of in vivo research with human participants. The facts that CD8+ T-cells quantitatively dominate in MS brain lesions and show distinctive features of clonal expansion and temporal persistence have suggested an important role of CD8+ T-cells in human MS. Recent technological advances, including multidimensional immune phenotyping and single-cell genome-wide transcriptomics, are expected to offer new insights regarding the role of different types of T cells. Striving for an increasingly better understanding of T cells in human MS is worthwhile as these cells are key drivers not only in MS but also in other neuro-immunological diseases.

Funding: RH receives research grant support by the German Research Foundation (DFG; SFB-TRR128; SyNergy, EXC 1010), German Ministry for Education and Research (BMBF; German Competence Network Multiple Sclerosis), Cyliax Stiftung and “Verein Therapieforschung für Multiple Sklerose Kranke“.
Conflicts of interest: RH has received grant support from Biogen, Novartis, Teva and personal fees from Actelion, Biogen, Genzyme-Sanofi, Immunic, Medday, Merck-Serono, Novartis, Roche, and Teva.

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Supporting Publications
Organised by
 
  • Elsevier
  • TLP
  • TLN
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  • Autoimmune Encephalitis (AE) Alliance
  • Encephalitis Society
  • Treating Autism
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