Rebound of disease activity after fingolimod withdrawal: Immunological and gene expression profiling.

[1]  C. Tornatore,et al.  Fingolimod Rebound: A Review of the Clinical Experience and Management Considerations , 2019, Neurology and Therapy.

[2]  S. Schmidt,et al.  Severe rebound after cessation of fingolimod treated with ocrelizumab with coincidental transient aggravation: report of two cases , 2019, Therapeutic advances in neurological disorders.

[3]  V. Meca-Lallana,et al.  Tumefactive multiple sclerosis lesions associated with fingolimod treatment: Report of 5 cases. , 2018, Multiple sclerosis and related disorders.

[4]  F. Quintana,et al.  Regulation of the Immune Response by the Aryl Hydrocarbon Receptor. , 2018, Immunity.

[5]  A. Bar-Or,et al.  Reconstitution of the peripheral immune repertoire following withdrawal of fingolimod , 2017, Multiple sclerosis.

[6]  E. Waubant,et al.  Rebound Syndrome in Patients With Multiple Sclerosis After Cessation of Fingolimod Treatment. , 2016, JAMA neurology.

[7]  L. Kappos,et al.  Long-term effects of fingolimod in multiple sclerosis , 2015, Neurology.

[8]  J. Kira,et al.  Peripheral Blood T Cell Dynamics Predict Relapse in Multiple Sclerosis Patients on Fingolimod , 2015, PloS one.

[9]  Fan Yang,et al.  STAT5 programs a distinct subset of GM-CSF-producing T helper cells that is essential for autoimmune neuroinflammation , 2014, Cell Research.

[10]  L. Kappos,et al.  Th17 central memory T cells are reduced by FTY720 in patients with multiple sclerosis , 2010, Neurology.

[11]  V. Brinkmann.  FTY720 (fingolimod) in Multiple Sclerosis: therapeutic effects in the immune and the central nervous system , 2009, British journal of pharmacology.

[12]  L. Kappos,et al.  FTY720 therapy exerts differential effects on T cell subsets in multiple sclerosis , 2008, Neurology.

[13]  L. Cosmi,et al.  Phenotypic and functional features of human Th17 cells , 2007, The Journal of experimental medicine.

[14]  R. Proia,et al.  Lymphocyte egress from thymus and peripheral lymphoid organs is dependent on S1P receptor 1 , 2004, Nature.