Several studies, including gene-fate mapping studies [54, 55], have now provided convincing evidence that most Th cells have a great degree of flexibility in their differentiation options. In the human system, it has been shown that Treg cells could acquire the CHIR-99021 in vivo capacity to produce IL-17, while maintaining the capacity to suppress T-cell effector functions [56, 57], while Th17 cells from the synovial fluid of oligoarticular-onset juvenile idiopathic arthritic patients shift in vitro from a Th17 to a Th17/Th1 or Th1 phenotype [58]. The time-dependent regulation of IL-17 and IL-10 production in Th17 cells that was discussed

above [37] may be considered as yet another example of Th-cell flexibility that underlines the robust and adaptive behavior of effector T cells in the immune response. The extent to which the immune system uses this flexibility and the consequences for

protection or immunopathology remain poorly understood and represent a challenge and an opportunity for future studies. The work in the authors’ laboratories is supported by grants from the Swiss National Science Foundation (N. 131092 to F.S. AZD8055 supplier and 126027 to A.L.) and the European Research Council. The Institute for Research in Biomedicine is supported by the Helmut Horten Foundation The authors declare no financial or commercial conflict of interest. “
“Multiple sclerosis (MS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) represent chronic, autoimmune demyelinating disorders of the central and peripheral Cytidine deaminase nervous system. Although both disorders share some fundamental pathogenic elements, treatments do not provide uniform effects across both disorders. We aim at providing an overview of current and future disease-modifying strategies in these disorders to demonstrate communalities and distinctions. Intravenous immunoglobulins (IVIG) have demonstrated short- and long-term beneficial effects in CIDP but are not effective in MS. Dimethyl fumarate (BG-12), teriflunomide and laquinimod are orally administered immunomodulatory

drugs that are already approved or likely to be approved in the near future for the basic therapy of patients with relapsing–remitting MS (RRMS) due to positive results in Phase III clinical trials. However, clinical trials with these drugs in CIDP have not (yet) been initiated. Natalizumab and fingolimod are approved for the treatment of RRMS, and trials to evaluate their safety and efficacy in CIDP are now planned. Alemtuzumab, ocrelizumab and daclizumab respresent monoclonal antibodies in advanced stages of clinical development for their use in RRMS patients. Attempts to study the safety and efficacy of alemtuzumab and B cell-depleting anti-CD20 antibodies, i.e. rituximab, ocrelizumab or ofatumumab, in CIDP patients are currently under way. We provide an overview of the mechanism of action and clinical data available on disease-modifying immunotherapy options for MS and CIDP.