Tobias V. Lanz

TL;DR: It was found that a first exposure of mice to LPS activated the ligand-operated transcription factor aryl hydrocarbon receptor and the hepatic enzyme tryptophan 2,3-dioxygenase, which provided an activating ligand to the former, to downregulate early inflammatory gene expression, pointing to a role for AhR in contributing to host fitness.

TL;DR: It is observed that RAAS is up-regulated in brain lesions of MS and its animal model, experimental autoimmune encephalomyelitis, and modulation of the RAAS with inexpensive, safe pharmaceuticals used by millions worldwide is an attractive therapeutic strategy for application to human autoimmune diseases.

TL;DR: In this paper , the authors demonstrate high-affinity molecular mimicry between the EBV transcription factor EBV nuclear antigen 1 (EBNA1) and the central nervous system protein glial cell adhesion molecule (GlialCAM) and provide structural and in vivo functional evidence for its relevance.

TL;DR: In this paper , the authors demonstrate high-affinity molecular mimicry between the EBV transcription factor EBV nuclear antigen 1 (EBNA1) and the central nervous system protein glial cell adhesion molecule (GlialCAM) and provide structural and in vivo functional evidence for its relevance.

TL;DR: Ang II is identified as a paracrine mediator, sustaining inflammation in the CNS in the EAE mouse model of MS via TGF-beta, suggesting that AT1R antagonists, frequently prescribed as antihypertensives, may be useful to interrupt this proinflammatory, CNS-specific pathway in individuals with MS.