Research Group Leader - Anneli Peters
Adaptive immune responses in CNS autoimmunity
2017 - present: Emmy Noether group leader at the Institute of Clinical Neuroimmunology, LMU, Munich, Germany
2014 - 2017: Project leader in Neuroimmunology at Max Planck Institute of Neurobiology, Munich, Germany
2010 - 2014: Research fellow at Center for Neurologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, USA
2007 - 2010: Ph.D. program at Ruhr-University Bochum, Germany and Center for Neurologic Diseases, Harvard Medical School, Boston, USA
2004 - 2006: Master of Science in Biochemistry at Ruhr-University Bochum, Germany and Center for Neurologic Diseases, Harvard Medical School, Boston, USA
Multiple Sclerosis (MS) is an autoimmune disease driven by self-reactive T helper (Th) cells, particularly Th1 and Th17 effector subsets, which promote tissue inflammation in the central nervous system (CNS). Research efforts both in MS patients, as well as in the animal model, experimental autoimmune encephalomyelitis (EAE), have largely focused on T cells. However, recent therapeutic advances highlight the importance of B cells for disease development and progression. Notably, we discovered that Th17 cells attract B cells, and induce formation of ectopic lymphoid follicles (eLFs) in the CNS during EAE, suggesting that B cells and Th17 cells cooperate in pathogenic inflammatory processes. Therefore, we are investigating the interplay between autoantigen-specific B and Th17 cells during disease initiation and progression using spontaneous transgenic mouse models, as well as adoptive transfer EAE. We are interested in the underlying mechanisms of how Th17 cells shape a pathogenic B cell response, and – vice versa - how B cells can support a pathogenic Th17 response. Our research aims to provide insight into the cellular mechanisms and kinetics of disease and may enable development of more tailored therapeutic strategies in the future.
List of Publications:
Mitsdoerffer M*, Peters A*. (2016). Tertiary Lymphoid Organs in Central Nervous System Autoimmunity. Front Immunol 7, 451.
Peters A*, Fowler KD*, Chalmin F, Merkler D, Kuchroo VK, Pot C. (2015). IL-27 induces Th17 differentiation in the absence of STAT1 signaling. J Immunol. 195, 4144-53.
Peters A*, Burkett PR*, Sobel RA, Buckley CD, Watson SP, Bettelli E, Kuchroo VK. (2015). Podoplanin negatively regulates CD4+ effector T cell responses. J Clin Invest. 125, 129-40.
Peters A, Yosef N. (2014). Understanding Th17 cells through systematic genomic analyses. Curr Opin Immunol. 28, 42-8.
Peters A, Pitcher LA, Sullivan JM, Mitsdoerffer M, Acton SE, Franz B, Wucherpfennig K, Turley S, Carroll MC, Sobel RA, Bettelli E, Kuchroo VK. (2011). Th17 cells induce ectopic lymphoid follicles in CNS tissue inflammation. Immunity. 35, 986-96.
Peters A, Lee Y, Kuchroo VK. (2011). The many faces of Th17 cells. Curr Opin Immunol. 23, 702-6.
Jäger A., V. Dardalhon, R.A. Sobel, E. Bettelli, V.K. Kuchroo. (2009). Th1, Th17, and Th9 effector cells induce experimental autoimmune encephalomyelitis with different pathological phenotypes. J Immunol. 183, 7169-77.
Awasthi A.*, L. Riol-Blanco*, A. Jäger*, T. Korn, C. Pot, G. Galileos, E. Bettelli, V.K. Kuchroo, M. Oukka. (2009). Cutting edge: IL-23 receptor gfp reporter mice reveal distinct populations of IL-17-producing cells. J Immunol. 182, 5904-8.
Korn T.*, E. Bettelli*, W. Gao*, A. Awasthi, A. Jäger, T.B. Strom, M. Oukka, V.K. Kuchroo. (2007). IL-21 initiates an alternative pathway to induce proinflammatory T(H)17 cells. Nature. 448, 484-7.
*These authors contributed equally.