Our Lab

Adaptive immune responses in CNS autoimmunity, Emmy Noether group

Welcome to the lab of Anneli Peters, PhD



Group photo

Our Aim

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. 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.

Our Approach

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.

To analyze T and B cell responses we employ different techniques including flow cytometry, ELISA and quantitative PCR. In addition, we visualize and analyze T:B cell interactions in the tissues via confocal and intravital microscopy (collaboration with 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.

Our Support

Our research is mainly funded by the Emmy Noether Programme from the German Research Foundation. Additionally we are supported by the ARSEP foundation and are associated with the SFB/TR128: Initiating/effector versus regulatory mechanisms in Multiple Sclerosis – progress towards tackling the disease. PhD candidates can apply to the IMPRS Program.