title: Abnormal Tr1 differentiation in multiple sclerosis.
abstract: Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS). In the recent years, accumulating evidence has supported an immunosuppressive role for regulatory T cells (Tregs). Most studies in the context of autoimmunity have focused on the defects of the CD4+CD25 high Tregs. However, we recently demonstrated an altered function of Tr1 Treg cells in MS, characterized by a lack of IL-10 secretion. Therefore, several major regulatory T cell defects are involved in human autoimmune disease. Hence, the induction of Tregs or the stimulation of Treg activity may be beneficial for the treatment of such diseases.
authors.affiliation: Laboratory of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. a.astier@ed.ac.uk
authors.forename: Anne L
authors.initials: AL
authors.lastname: Astier
authors.forename: David A
authors.initials: DA
authors.lastname: Hafler
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D015654:Herpesvirus 6, Human / Q000502:physiology; D006801:Humans; D016753:Interleukin-10 / Q000096:biosynthesis; D008213:Lymphocyte Activation; D051916:Membrane Cofactor Protein / Q000502:physiology*; D009103:Multiple Sclerosis / Q000276:immunology*; D020033:Protein Isoforms; D050378:T-Lymphocytes, Regulatory / Q000166:cytology / Q000276:immunology / Q000502:physiology*
chemical_list: D051916:Membrane Cofactor Protein; D020033:Protein Isoforms; D016753:Interleukin-10