Peters Lab – T:B cell interactions
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 both in the CNS and in the periphery. We are interested in the underlying mechanisms of how T cells shape a pathogenic B cell response, and – vice versa - how B cells can support a pathogenic T cell 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.
We are utilizing transgenic mouse models, which express an autoantigen-specific T cell receptor and spontaneously develop B cell-dependent disease, either with an acute-chronic or a relapsing-remitting disease course. Spontaneous models are particularly useful for studying the initial T:B cell interactions. We also induce EAE by adoptive transfer in order to be able to differentiate between Th1 and Th17 effects and to study both pathogenic and regulatory effects of B cells.
To analyze T and B cell responses we employ different techniques including multi-parameter flow cytometry, ELISA, quantitative PCR and NGS (in collaboration with the Dornmair Lab). In addition, we visualize and analyze T:B cell interactions in the tissues via confocal and intravital microscopy (in collaboration with the Kawakami Lab). With our cell culture systems we can manipulate T and B cells, in order to gain insight into the molecular basis of pathogenic properties.
Benakis C, Simats A, Tritschler S, Heindl S, Besson-Girard S, Llovera G, Pinkham K, Kolz A, Ricci A, Theis FJ, Bittner S, Gökce Ö, Peters A, Liesz A. T cells modulate the microglial response to brain ischemia. Elife. 2022 Dec 13;11:e82031.
Salvador F, Deramoudt L, Leprêtre F, Figeac M, Guerrier T, Boucher J, Bas M, Journiac N, Peters A, Mars LT, Zéphir H. A Spontaneous Model of Experimental Autoimmune Encephalomyelitis Provides Evidence of MOG-Specific B Cell Recruitment and Clonal Expansion. Front Immunol. 2022 Feb 3;13:755900.
Hartlehnert M, Börsch AL, Li X, Burmeister M, Gerwien H, Schafflick D, Heming M, Lu IN, Narayanan V, Strecker JK, Kolz A, Peters A, Wu GF, Wiendl H, Sorokin L, Meyer Zu Horste G. Bcl6 controls meningeal Th17-B cell interaction in murine neuroinflammation. Proc Natl Acad Sci U S A. 2021 Sep 7;118(36):e2023174118.
Gerdes LA, Yoon H, Peters A. Mikrobiota und Multiple Sklerose [Microbiota and multiple sclerosis]. Nervenarzt. 2020 Oct 12. German.
Matthias J, Heink S, Picard F, Zeiträg J, Kolz A, Chao YY, Soll D, de Almeida GP, Glasmacher E, Jacobsen ID, Riedel T, Peters A, Floess S, Huehn J, Baumjohann D, Huber M, Korn T, Zielinski CE. Salt generates antiinflammatory Th17 cells but amplifies pathogenicity in proinflammatory cytokine microenvironments. J Clin Invest. 2020 Sep 1;130(9):4587-4600.
Peters A, Wekerle H. Autoimmune diabetes mellitus and the leaky gut. Proc Natl Acad Sci U S A. 2019 Jul 23;116(30):14788-14790.
Mitsdoerffer M, Peters A. Tertiary Lymphoid Organs in Central Nervous System Autoimmunity. Front Immunol. 2016 Oct 25;7:451.
Peters A, Burkett PR, Sobel RA, Buckley CD, Watson SP, Bettelli E, Kuchroo VK. Podoplanin negatively regulates CD4+ effector T cell responses. J Clin Invest. 2015 Jan;125(1):129-40.
Peters A, Fowler KD, Chalmin F, Merkler D, Kuchroo VK, Pot C. IL-27 Induces Th17 Differentiation in the Absence of STAT1 Signaling. J Immunol. 2015 Nov 1;195(9):4144-53.
Peters A, Pitcher LA, Sullivan JM, Mitsdoerffer M, Acton SE, Franz B, Wucherpfennig K, Turley S, Carroll MC, Sobel RA, Bettelli E, Kuchroo VK. Th17 cells induce ectopic lymphoid follicles in central nervous system tissue inflammation. Immunity. 2011 Dec 23;35(6):986-96.
Anna Thomann, PhD student
I studied Biomedicine at the Julius-Maximilians-Universität Würzburg and received my master degree in 2017. I was always interested in autoimmune diseases, which is why I went to the US during my studies, where I did research on myasthenia gravis and the microbiome in multiple sclerosis. I started my PhD at the Institute of Clinical Neuroimmunology in 2017 and for my thesis, I’m investigating the role of cytokine-producing B cells in the initiation and regulation of EAE. In my free time, I like playing volleyball, singing or meeting friends.
Anna Kolz, PhD student
My project focuses on the interaction of Th17 cells and B cells in ectopic lymphoid follicle-like structures (eLFs), which form under the meninges in our adoptive transfer EAE mouse model. As these structures have also been described in MS patients, the aim of my project is to analyze the cellular processes inside eLFs. As an IMPRS-LS student, I enjoy the scientific and cultural exchange in the international community of fellow PhD students. In my free time, I love swimming, traveling and exploring the lakes and mountains of the Munich area.
Hongsup Yoon, Postdoctoral fellow
I am from Busan in South Korea. I completed my PhD at the Technical University of Munich, where research focused on intestinal dysbiosis and immune responses in inflammatory bowel disease. Currently, I am working in the Emeritus group of Prof. Wekerle and Prof. Hohlfeld and, in collaboration with the clinical group (AG Kümpfel) and AG Peters, my project aims to understand how the intestinal microbiota influences inflammation in the gut and CNS using germ-free spontaneous EAE mouse model. Outside the lab, I enjoy spending time with my family and children.
Rosa Schmitz, PhD student
I studied medical Biology at the University Duisburg-Essen and figured out quite early that I want to do research in immunology. The complexity of the immune system fascinates me and autoimmune diseases like multiple sclerosis (MS) underline the importance of an effective regulation of the immune system. In my PhD project I want to investigate the mechanism of action of different B-cell directed therapies in murine MS models. Do they alter the interaction of different immune cell subsets and influence the formation of ectopic lymphoid follicles in the central nervous system?
Besides trying to answer these questions, I do horse riding and love to cook and bake for friends and family.
Jiancheng Wang, MD studentI finished my master and residency in West China Hospital of Sichuan University. During my master study, I managed and followed up a lot of patients with MS and NMOSD. In my mind, it is important to find the mechanisms of diseases for so many patients suffering from these diseases while few of them could be cured. After my master study, I started my MD thesis in Dr. Peters’ and Dr. Gerdes’ lab and the aim of my project is to figure out how gut microbiota may trigger multiple sclerosis. In my free time, I love playing tennis and cooking Chinese food with friends.
Courtney McQuade, PhD student
Mathias Linnerbauer, PhD student, FAU Erlangen
Monika Schaubeck, Scientist, Hipp
Klaus Hämäläinen, Pharmacist, Helsinki
Dr. rer. nat Anneli Peters
Even though I am a biochemist by training I discovered my passion for immunology early during my master thesis, which I conducted at the Center for Neurologic Diseases, Harvard Medical School in Boston. Fascinated by the topic, I stayed for my PhD and investigated the role different T helper cell subsets play in the induction of CNS autoimmunity. We discovered that Th17 cells can induce formation of ectopic lymphoid follicle-like structures in the CNS meninges (Immunity, 2011), and further contributed to characterize properties of Th17 cells, a subset that is implicated not only in MS but also in many other autoimmune diseases (JI, 2015; JCI 2015). Back in Germany I became interested in the role of B cells in spontaneous EAE at the MPI of Neurobiology. Being awarded an Emmy Noether grant, I started my own lab at the Institute of Clinical Neuroimmunology, LMU, to study T:B cell interactions in the initiation and progression of CNS autoimmunity.
I enjoy the positive energy of our young team and am looking forward to exciting discoveries!
2001 – 2004 Bachelor of Science in Biochemistry, Ruhr-University Bochum, Germany
2004 – 2006 Master of Science in Biochemistry, Ruhr-University Bochum, Germany and Center for Neurologic Diseases, Harvard Medical School, Boston, USA
2007 – 2010 Ph.D. program at Ruhr-University Bochum, Germany and Center for Neurologic Diseases, Harvard Medical School, Boston, USA (summa cum laude)
2010 – 2014 Research fellow at Harvard Medical School and Brigham and Women's Hospital, Boston, USA
Academic positions & appointments
2014 – 2017 Project leader at Max Planck Institute of Neurobiology, Munich, Germany
since 2017 Emmy Noether group leader at the Institute of Clinical Neuroimmunology, LMU, Munich
since 2017 Associated junior faculty member of the International Max Planck Research School for Molecular and Cellular Life Sciences (IMPRS-LS)
Awards & honors
2001 – 2003 Anniversary Scholarship by the German Chemical Industry Fund
2006 DAAD scholarship for conducting a master thesis project abroad
2007 – 2010 Boehringer Ingelheim Fonds Ph.D. scholarship
2012 – 2013 Postdoctoral fellowship from the German Multiple Sclerosis society (DMSG)
2012 Multiple Sclerosis Young Investigator Award from the Eva and Helmer Lehmann foundation
2017 awarded an Emmy Noether grant by the German Research Foundation (DFG)
2017 Junior scientist award of the Roman, Marga und Mareille Sobek-Stiftung for Multiple Sclerosis Research
Defense Anna K 2022
BMC Advent calendar 2021
PhD hat artwork
Defense Anna T 2022
Proud PhD! Anna K 2022
November 2020: masks everywhere…
We gratefully acknowledge support for our work by the following agencies:
Friedrich Bauer Stiftung