Abnormal Tr1 differentiation in multiple sclerosis.
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.
Astier
Anne L
AL
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
Hafler
David A
DA
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*
D051916:Membrane Cofactor Protein; D020033:Protein Isoforms; D016753:Interleukin-10