Research interests

Despite the fact that the central nervous system (CNS) is considered an immune privileged organ and central tolerance is supposed to eliminate self-reactive T cell clones, myelin-reactive T cell responses drive CNS autoimmunity in multiple sclerosis (MS). We are interested in cellular and molecular mechanisms that regulate disease initiation and progression. Tryptophan metabolism is a key process that shapes immunosuppressive T cell responses and we have shown that downstream signaling indeed limits autoimmune neuroinflammation. In addition, we are currently investigating the impact of the gut microbiome composition on encephalitogenic  T cell responses. Delineating the complex interplay between the microbiome, antigen presentation and T cell activation will eventually help us to develop novel strategies for MS therapy. 

After vaccination with immungenic peptides derived from myelin proteins autoreactive T cells penetrate the blood-brain-barrier and infiltrate the central nervous system (CNS). Encephalitogenic T cells, infiltrating macrophages and brain-resident microglia release soluble factors that mediate demyelination and cause ascending paralysis. During the remission phase regulatory T cells accumulate within the inflammatory lesions in the CNS where they dampen autoreactive T cell responses. It is widely accepted that changes within the gut microbiome composition have a profound effect on immune responses within both the local tissue microenvironment and remote tissues such as the CNS. However, the exact mechanisms of how alterations in the regulation of immune responses within gut are transmitted to the CNS via the gut-brain-axis remain poorly understood.
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Team members

  • Jana Sonner
  • Magdalena Kramer
  • Julian Röwe
  • Lara Wolf


  • Lanz TV, Becker S, Mohapatra SR, Opitz CA, Wick W, Platten M (2017). Suppression of Th1 differentiation by tryptophan supplementation in vivo. Amino Acids; 49, 1169-1175. doi: 10.1007/s00726-017-2415-4.
  • Lanz TV, Williams SK, Stojic A, Iwantscheff S, Sonner JK, Grabitz C, Becker S, Böhler LI, Mohapatra SR, Sahm F, Küblbeck G, Nakamura T, Funakoshi H, Opitz CA, Wick W, Diem R, Platten M (2017). Tryptophan-2,3-Dioxygenase (TDO) deficiency is associated with subclinical neuroprotection in a mouse model of multiple sclerosis. Sci Rep; 24, 7:41271. doi: 10.1038/srep41271.
  • Keil M, Sonner JK, Lanz TV, Oezen I, Bunse T, Bittner S, Meyer HV, Meuth SG, Wick W, Platten M (2016). General control non-derepressible 2 (GCN2) in T cells controls disease progression of autoimmune neuroinflammation. J Neuroimmunol; 15, 117-126. doi: 10.1016/j.jneuroim.2016.05.014.
  • Lanz TV, Becker S, Osswald M, Bittner S, Schumacher MK, Opitz CA, Gaikwad S, Wiestler B, Litzenburger UM, Sahm F, Ott M, Iwantscheff S, Grabitz C, Mittelbronn M, von Deimling A, Winkler F, Meuth SG, Wick W, Platten M (2013). Protein kinase Cβ as a therapeutic target stabilizing blood-brain barrier disruption in experimental autoimmune encephalomyelitis. Proc Natl Acad Sci U S A; 3, 14735-14740. doi: 10.1073/pnas.1302569110.
  • Lanz TV, Opitz CA, Ho PP, Agrawal A, Lutz C, Weller M, Mellor AL, Steinman L, Wick W, Platten M (2009). Mouse Mesenchymal Stem Cells Suppress Antigen-Specific TH Cell Immunity Independent of Indoleamine 2,3-Dioxygenase 1 (IDO1). Stem Cell Dev; 19, 657-668. doi:  10.1089/scd.2009.0385.


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