644
Views
42
CrossRef citations to date
0
Altmetric
Theme: Demyelinating Diseases - Review

Treating multiple sclerosis with monoclonal antibodies: a 2013 update

, , &
Pages 313-335 | Published online: 09 Jan 2014

References

  • Buttmann M. Treating multiple sclerosis with monoclonal antibodies: a 2010 update. Expert Rev. Neurother. 10(5), 791–809 (2010).
  • Buttmann M, Rieckmann P. Treating multiple sclerosis with monoclonal antibodies. Expert Rev. Neurother. 8(3), 433–455 (2008).
  • Iaffaldano P, Lucchese G, Trojano M. Treating multiple sclerosis with natalizumab. Expert Rev. Neurother. 11(12), 1683–1692 (2011).
  • Pucci E, Giuliani G, Solari A et al. Natalizumab for relapsing remitting multiple sclerosis. Cochrane Database Syst. Rev. 10, CD007621 (2011).
  • Costelloe L, Jones J, Coles A. Secondary autoimmune diseases following alemtuzumab therapy for multiple sclerosis. Expert Rev. Neurother. 12(3), 335–341 (2012).
  • Klotz L, Meuth SG, Wiendl H. Immune mechanisms of new therapeutic strategies in multiple sclerosis-A focus on alemtuzumab. Clin. Immunol. 142(1), 25–30 (2012).
  • Fox EJ. Alemtuzumab in the treatment of relapsing–remitting multiple sclerosis. Expert Rev. Neurother. 10(12), 1789–1797 (2010).
  • Liu J, Wang L, Zhan SY, Xia Y. Daclizumab for relapsing remitting multiple sclerosis. Cochrane Database Syst. Rev. 4, CD008127 (2012).
  • Martin R. Anti-CD25 (daclizumab) monoclonal antibody therapy in relapsing–remitting multiple sclerosis. Clin. Immunol. 142(1), 9–14 (2012).
  • Stüve O, Greenberg BM. Anticipated benefits and surprising effects of daclizumab in multiple sclerosis. Lancet Neurol. 9(4), 337–338 (2010).
  • Barun B, Bar-Or A. Treatment of multiple sclerosis with anti-CD20 antibodies. Clin. Immunol. 142(1), 31–37 (2012).
  • He D, Zhou H, Han W, Zhang S. Rituximab for relapsing–remitting multiple sclerosis. Cochrane Database Syst. Rev. 12, CD009130 (2011).
  • Bartok B, Silverman GJ. Development of anti-CD20 therapy for multiple sclerosis. Exp. Cell Res. 317(9), 1312–1318 (2011).
  • Gensicke H, Leppert D, Yaldizli Ö et al. Monoclonal antibodies and recombinant immunoglobulins for the treatment of multiple sclerosis. CNS Drugs 26(1), 11–37 (2012).
  • Bloomgren G, Richman S, Hotermans C et al. Risk of natalizumab-associated progressive multifocal leukoencephalopathy. N. Engl. J. Med. 366(20), 1870–1880 (2012).
  • Bozic C, Subramanyam M, Paes D et al. Anti-JC virus antibody prevalence in the JCV Epidemiology in MS trial. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P824, 10–13 October 2012.
  • Van Assche G, Van Ranst M, Sciot R et al. Progressive multifocal leukoencephalopathy after natalizumab therapy for Crohn’s disease. N. Engl. J. Med. 353(4), 362–368 (2005).
  • Vermersch P. Epidemiology of natalizumab-associated PML and IRIS in MS. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, 98, 10–13 October 2012.
  • Richert N, Bloomgren G, Cadavid D, Dong-Si T, Richman S, Ticho B. Imaging findings for PML in natalizumab-treated MS patients. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, 99, 10–13 October 2012.
  • Yousry TA, Pelletier D, Cadavid D et al. Magnetic resonance imaging pattern in natalizumab-associated progressive multifocal leukoencephalopathy. Ann. Neurol. 72(5), 779–787 (2012).
  • Vermersch P, Kappos L, Gold R et al. Clinical outcomes of natalizumab-associated progressive multifocal leukoencephalopathy. Neurology 76(20), 1697–1704 (2011).
  • Kappos L, Bates D, Edan G et al. Natalizumab treatment for multiple sclerosis: updated recommendations for patient selection and monitoring. Lancet Neurol. 10(8), 745–758 (2011).
  • Langer-Gould A, Atlas SW, Green AJ, Bollen AW, Pelletier D. Progressive multifocal leukoencephalopathy in a patient treated with natalizumab. N. Engl. J. Med. 353(4), 375–381 (2005).
  • Antoniol C, Jilek S, Schluep M et al. Impairment of JCV-specific T-cell response by corticotherapy: effect on PML-IRIS management? Neurology 79(23), 2258–2264 (2012).
  • Kleinschmidt-DeMasters BK, Miravalle A, Schowinsky J, Corboy J, Vollmer T. Update on PML and PML-IRIS occurring in multiple sclerosis patients treated with natalizumab. J. Neuropathol. Exp. Neurol. 71(7), 604–617 (2012).
  • Sørensen PS, Bertolotto A, Edan G et al. Risk stratification for progressive multifocal leukoencephalopathy in patients treated with natalizumab. Mult. Scler. 18(2), 143–152 (2012).
  • Cohen JA, Coles AJ, Arnold DL et al.; CARE-MS I investigators. Alemtuzumab versus interferon β1a as first-line treatment for patients with relapsing–remitting multiple sclerosis: a randomised controlled Phase 3 trial. Lancet 380(9856), 1819–1828 (2012).
  • Coles AJ, Fox E, Vladic A et al. Alemtuzumab more effective than interferon b-1a at 5-year follow-up of CAMMS223 clinical trial. Neurology 78(14), 1069–1078 (2012).
  • Keene DL, Legare C, Taylor E, Gallivan J, Cawthorn GM, Vu D. Monoclonal antibodies and progressive multifocal leukoencephalopathy. Can. J. Neurol. Sci. 38(4), 565–571 (2011).
  • Phan-Ba R, Belachew S, Outteryck O et al. The earlier, the smaller, the better for natalizumab-associated PML: in MRI vigilance veritas? Neurology 79(10), 1067–1069 (2012).
  • Blair NF, Brew BJ, Halpern JP. Natalizumab-associated PML identified in the presymptomatic phase using MRI surveillance. Neurology 78(7), 507–508 (2012).
  • Ayzenberg I, Lukas C, Trampe N, Gold R, Hellwig K. Value of MRI as a surrogate marker for PML in natalizumab long-term therapy. J. Neurol. 259(8), 1732–1733 (2012).
  • Phan-Ba R, Lommers E, Tshibanda L et al. MRI preclinical detection and asymptomatic course of a progressive multifocal leucoencephalopathy (PML) under natalizumab therapy. J. Neurol. Neurosurg. Psychiatr. 83(2), 224–226 (2012).
  • Bozic C, Richman S, Plavina T et al. Anti-John Cunnigham virus antibody prevalence in multiple sclerosis patients: baseline results of STRATIFY-1. Ann. Neurol. 70(5), 742–750 (2011).
  • Gorelik L, Lerner M, Bixler S et al. Anti-JC virus antibodies: implications for PML risk stratification. Ann. Neurol. 68(3), 295–303 (2010).
  • Trampe AK, Hemmelmann C, Stroet A et al. Anti-JC virus antibodies in a large German natalizumab-treated multiple sclerosis cohort. Neurology 78(22), 1736–1742 (2012).
  • Lanzillo R, Liuzzi R, Guacci A et al. JCV antibodies seroconversion on natalizumab treatment and predictive factors: preliminary data. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P539, 10–13 October 2012.
  • Etxeberria A, Outteryck O, Ongagna JC et al. Annual rate of JCV seroconversion in a French Cohort of MS Patients under Natalizumab. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P996, 10–13 October 2012.
  • Haghikia A, Perrech M, Pula B et al. Functional energetics of CD4+-cellular immunity in monoclonal antibody-associated progressive multifocal leukoencephalopathy in autoimmune disorders. PLoS ONE 6(4), e18506 (2011).
  • Goelz S, Polman C, Rudick R et al. ImmuKnow® (Cylex) does not appear to be useful for PML risk stratification with natalizumab treatment. Presented at: 5th Joint Triennial Congress of the European and Americas Committees for Treatment and Research in Multiple Sclerosis. Amsterdam, The Netherlands, P1118, 19–22 October 2011.
  • Zahednasab H. Anti-JC virus antibodies in a large German natalizumab-treated MS cohort. Neurology 79(19), 2010; author reply 2010–2010; author reply 2011 (2012).
  • Laroni A, Giacomazzi CG, Grimaldi L et al. Urinary JCV-DNA testing during natalizumab treatment may increase accuracy of PML risk stratification. J. Neuroimmune Pharmacol. 7(3), 665–672 (2012).
  • O’Connor PW, Goodman A, Kappos L et al. Disease activity return during natalizumab treatment interruption in patients with multiple sclerosis. Neurology 76(22), 1858–1865 (2011).
  • Sangalli F, Moiola L, Ferrè L et al. Long-term observation on management of natalizumab discontinuation. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P977, 10–13 October 2012.
  • Clerico M, De Mercanti S, Piazza F et al. Looking for the best therapeutical strategy after the 24th natalizumab administration. The TY-STOP study. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P976, 10–13 October 2012.
  • Papeix C, Vukusic S, Passante N et al. Natalizumab discontinuation in clinical practice: a systematic observational study from the national TYSEDMUS cohort of 577 multiple sclerosis patients treated with natalizumab in France. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P1004, 10–13 October 2012.
  • Rinaldi F, Seppi D, Calabrese M, Perini P, Gallo P. Switching therapy from natalizumab to fingolimod in relapsing–remitting multiple sclerosis: clinical and magnetic resonance imaging findings. Mult. Scler. 18(11), 1640–1643 (2012).
  • Jander S, Turowski B, Kieseier BC, Hartung HP. Emerging tumefactive multiple sclerosis after switching therapy from natalizumab to fingolimod. Mult. Scler. 18(11), 1650–1652 (2012).
  • Centonze D, Rossi S, Rinaldi F, Gallo P. Severe relapses under fingolimod treatment prescribed after natalizumab. Neurology 79(19), 2004–2005 (2012).
  • Daelman L, Maitrot A, Maarouf A, Chaunu MP, Papeix C, Tourbah A. Severe multiple sclerosis reactivation under fingolimod 3 months after natalizumab withdrawal. Mult. Scler. 18(11), 1647–1649 (2012).
  • Ghezzi A, Baroncini D, Annovazzi PO, Bianchi A, Minonzio G, Comi G. From natalizumab to fingolimod: an observational study of 32 patients. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P938, 10–13 October 2012.
  • Ongagna JC, Courtois S, Gaultier C et al. Therapeutic decision after JC virus testing in a cohort of patients treated with natalizumab. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P496, 10–13 October 2012.
  • Tur C, Tintoré M, Vidal-Jordana A et al. Natalizumab discontinuation after PML risk stratification: outcome from a shared and informed decision. Mult. Scler. 18(8), 1193–1196 (2012).
  • Kappos L, Goodman A, Lublin F et al. Five-year safety and efficacy data of natalizumab from the STRATA study. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P520, 10–13 October 2012.
  • Bonig H, Wundes A, Chang KH, Lucas S, Papayannopoulou T. Increased numbers of circulating hematopoietic stem/progenitor cells are chronically maintained in patients treated with the CD49d blocking antibody natalizumab. Blood 111(7), 3439–3441 (2008).
  • Neumann F, Zohren F, Haas R. The role of natalizumab in hematopoietic stem cell mobilization. Expert Opin. Biol. Ther. 9(8), 1099–1106 (2009).
  • Saure C, Warnke C, Zohren F et al. Natalizumab and impedance of the homing of CD34+ hematopoietic progenitors. Arch. Neurol. 68(11), 1428–1431 (2011).
  • Kivisäkk P, Healy BC, Viglietta V et al. Natalizumab treatment is associated with peripheral sequestration of proinflammatory T cells. Neurology 72(22), 1922–1930 (2009).
  • Frisullo G, Iorio R, Plantone D et al. CD4+T-bet+, CD4+pSTAT3+ and CD8+T-bet+ T cells accumulate in peripheral blood during NZB treatment. Mult. Scler. 17(5), 556–566 (2011).
  • Ramos-Cejudo J, Oreja-Guevara C, Stark Aroeira L, Rodriguez de Antonio L, Chamorro B, Diez-Tejedor E. Treatment with natalizumab in relapsing–remitting multiple sclerosis patients induces changes in inflammatory mechanism. J. Clin. Immunol. 31(4), 623–631 (2011).
  • Khademi M, Bornsen L, Rafatnia F et al. The effects of natalizumab on inflammatory mediators in multiple sclerosis: prospects for treatment-sensitive biomarkers. Eur. J. Neurol. 16(4), 528–536 (2009).
  • Khademi M, Stol D, Olsson T, Wallström E. Induction of systemic TNFα in natalizumab-treated multiple sclerosis. Eur. J. Neurol. 15(3), 309–312 (2008).
  • Lindberg RL, Achtnichts L, Hoffmann F, Kuhle J, Kappos L. Natalizumab alters transcriptional expression profiles of blood cell subpopulations of multiple sclerosis patients. J. Neuroimmunol. 194(1–2), 153–164 (2008).
  • Stüve O, Marra CM, Jerome KR et al. Immune surveillance in multiple sclerosis patients treated with natalizumab. Ann. Neurol. 59(5), 743–747 (2006).
  • Stüve O, Marra CM, Bar-Or A et al. Altered CD4+/CD8+ T-cell ratios in cerebrospinal fluid of natalizumab-treated patients with multiple sclerosis. Arch. Neurol. 63(10), 1383–1387 (2006).
  • Benkert TF, Dietz L, Hartmann EM et al. Natalizumab exerts direct signaling capacity and supports a pro-inflammatory phenotype in some patients with multiple sclerosis. PLoS ONE 7(12), e52208 (2012).
  • Kerbrat A, Le Page E, Leray E et al. Natalizumab and drug holiday in clinical practice: an observational study in very active relapsing remitting multiple sclerosis patients. J. Neurol. Sci. 308(1–2), 98–102 (2011).
  • Vellinga MM, Castelijns JA, Barkhof F, Uitdehaag BM, Polman CH. Postwithdrawal rebound increase in T2 lesional activity in natalizumab-treated MS patients. Neurology 70(13 Pt 2), 1150–1151 (2008).
  • West TW, Cree BA. Natalizumab dosage suspension: are we helping or hurting? Ann. Neurol. 68(3), 395–399 (2010).
  • Rigau V, Mania A, Béfort P et al. Lethal multiple sclerosis relapse after natalizumab withdrawal. Neurology 79(22), 2214–2216 (2012).
  • Miravalle A, Jensen R, Kinkel RP. Immune reconstitution inflammatory syndrome in patients with multiple sclerosis following cessation of natalizumab therapy. Arch. Neurol. 68(2), 186–191 (2011).
  • Tan IL, McArthur JC, Clifford DB, Major EO, Nath A. Immune reconstitution inflammatory syndrome in natalizumab-associated PML. Neurology 77(11), 1061–1067 (2011).
  • Haarmann A, Nowak E, Stoll G, Berberich-Siebelt F, Buttmann M. Both soluble vascular cell adhesion molecule-1 and natalizumab actively modulate paracellular barrier function of cultured human brain endothelium via α4-integrin mediated intracellular signalling. Presented at: 5th Joint Triennial Congress of the European and Americas Committees for Treatment and Research in Multiple Sclerosis.Amsterdam, The Netherlands, P470, 19–22 October 2011.
  • Kallmann BA, Hummel V, Lindenlaub T, Ruprecht K, Toyka KV, Rieckmann P. Cytokine-induced modulation of cellular adhesion to human cerebral endothelial cells is mediated by soluble vascular cell adhesion molecule-1. Brain 123(Pt 4), 687–697 (2000).
  • Hartung HP, Reiners K, Archelos JJ et al. Circulating adhesion molecules and tumor necrosis factor receptor in multiple sclerosis: correlation with magnetic resonance imaging. Ann. Neurol. 38(2), 186–193 (1995).
  • Rieckmann P, Altenhofen B, Riegel A, Baudewig J, Felgenhauer K. Soluble adhesion molecules (sVCAM-1 and sICAM-1) in cerebrospinal fluid and serum correlate with MRI activity in multiple sclerosis. Ann. Neurol. 41(3), 326–333 (1997).
  • Rieckmann P, Altenhofen B, Riegel A, Kallmann B, Felgenhauer K. Correlation of soluble adhesion molecules in blood and cerebrospinal fluid with magnetic resonance imaging activity in patients with multiple sclerosis. Mult. Scler. 4(3), 178–182 (1998).
  • Coles AJ, Compston DA, Selmaj KW et al. Alemtuzumab vs. interferon β1a in early multiple sclerosis. N. Engl. J. Med. 359(17), 1786–1801 (2008).
  • Coles AJ, Twyman CL, Arnold DL et al.; CARE-MS II investigators. Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomised controlled Phase 3 trial. Lancet 380(9856), 1829–1839 (2012).
  • Polman CH, Reingold SC, Edan G et al. Diagnostic criteria for multiple sclerosis: 2005 revisions to the ‘McDonald Criteria’. Ann. Neurol. 58(6), 840–846 (2005).
  • Paolillo A, Coles AJ, Molyneux PD et al. Quantitative MRI in patients with secondary progressive MS treated with monoclonal antibody Campath 1H. Neurology 53(4), 751–757 (1999).
  • Jones JL, Coles AJ. Spotlight on alemtuzumab. Int. MS J. 16(3), 77–81 (2009).
  • Jones JL, Anderson JM, Phuah CL et al. Improvement in disability after alemtuzumab treatment of multiple sclerosis is associated with neuroprotective autoimmunity. Brain 133(Pt 8), 2232–2247 (2010).
  • Cossburn M, Pace AA, Jones J et al. Autoimmune disease after alemtuzumab treatment for multiple sclerosis in a multicenter cohort. Neurology 77(6), 573–579 (2011).
  • Hill-Cawthorne GA, Button T, Tuohy O et al. Long term lymphocyte reconstitution after alemtuzumab treatment of multiple sclerosis. J. Neurol. Neurosurg. Psychiatr. 83(3), 298–304 (2012).
  • Compston A. The nature of multiple sclerosis. Presented at: 11th International Congress of Neuroimmunology. Boston, MA, USA, 540, 4–8 November 2012.
  • Cossburn MD, Harding K, Ingram G et al. Clinical relevance of differential lymphocyte recovery after alemtuzumab therapy for multiple sclerosis. Neurology 80(1), 55–61 (2013).
  • Coles AJ, Cox A, Le Page E et al. The window of therapeutic opportunity in multiple sclerosis: evidence from monoclonal antibody therapy. J. Neurol. 253(1), 98–108 (2006).
  • Clatworthy MR, Wallin EF, Jayne DR. Anti-glomerular basement membrane disease after alemtuzumab. N. Engl. J. Med. 359(7), 768–769 (2008).
  • Sheridan C. Abbott outbids Biogen for Facet’s multiple sclerosis antibody. Nat. Biotechnol. 28(5), 387–389 (2010).
  • Wynn D, Kaufman M, Montalban X et al.; CHOICE investigators. Daclizumab in active relapsing multiple sclerosis (CHOICE study): a Phase 2, randomised, double-blind, placebo-controlled, add-on trial with interferon β. Lancet Neurol. 9(4), 381–390 (2010).
  • Bielekova B, Catalfamo M, Reichert-Scrivner S et al. Regulatory CD56(bright) natural killer cells mediate immunomodulatory effects of IL-2Rα-targeted therapy (daclizumab) in multiple sclerosis. Proc. Natl Acad. Sci. USA 103(15), 5941–5946 (2006).
  • Giovannoni G, Gold R, Selmaj K et al. Primary results of the SELECTION trial of daclizumab HYP in relapsing multiple sclerosis. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, 169, 10–13 October 2012.
  • Sheridan JP, Zhang Y, Riester K et al. Intermediate-affinity interleukin-2 receptor expression predicts CD56(bright) natural killer cell expansion after daclizumab treatment in the CHOICE study of patients with multiple sclerosis. Mult. Scler. 17(12), 1441–1448 (2011).
  • Buttmann M, Toyka KV. Can we get rid of neutralizing antibodies against interferon-b? Eur. J. Neurol. 16(1), 7–9 (2009).
  • Polman CH, Bertolotto A, Deisenhammer F et al. Recommendations for clinical use of data on neutralising antibodies to interferon-β therapy in multiple sclerosis. Lancet Neurol. 9(7), 740–750 (2010).
  • Giovannoni G, Gold R, Selmaj K et al. A randomized, double-blind, placebo-controlled study to evaluate the safety and efficacy of daclizumab HYP monotherapy in relapsing-remitting multiple sclerosis: primary results of the SELECT trial. Presented at: 5th Joint Triennial Congress of the European and Americas Committees for Treatment and Research in Multiple Sclerosis. Amsterdam, The Netherlands, 149, 19–22 October 2011.
  • Giovannoni G, Radue E-W, Havrdova E et al. Effect of daclizumab HYP treatment in highly active relapsing–remitting multiple sclerosis: results from the SELECT study. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P463, 10–13 October 2012.
  • Disanto G, Morahan JM, Barnett MH, Giovannoni G, Ramagopalan SV. The evidence for a role of B cells in multiple sclerosis. Neurology 78(11), 823–832 (2012).
  • Ireland SJ, Blazek M, Harp CT et al. Antibody-independent B cell effector functions in relapsing remitting multiple sclerosis: clues to increased inflammatory and reduced regulatory B cell capacity. Autoimmunity 45(5), 400–414 (2012).
  • Hauser SL, Waubant E, Arnold DL et al.; HERMES Trial Group. B-cell depletion with rituximab in relapsing–remitting multiple sclerosis. N. Engl. J. Med. 358(7), 676–688 (2008).
  • Hawker K, O’Connor P, Freedman MS et al.; OLYMPUS trial group. Rituximab in patients with primary progressive multiple sclerosis: results of a randomized double-blind placebo-controlled multicenter trial. Ann. Neurol. 66(4), 460–471 (2009).
  • Kappos L, Li D, Calabresi PA et al. Ocrelizumab in relapsing–remitting multiple sclerosis: a Phase 2, randomised, placebo-controlled, multicentre trial. Lancet 378(9805), 1779–1787 (2011).
  • McDonald WI, Compston A, Edan G et al. Recommended diagnostic criteria for multiple sclerosis: guidelines from the International Panel on the diagnosis of multiple sclerosis. Ann. Neurol. 50(1), 121–127 (2001).
  • Kappos L, Calabresi P, O’Connor P et al. Long-term safety and efficacy of ocrelizumab in patients with relapsing-remitting multiple sclerosis: week 144 results of a Phase II, randomised, multicentre trial. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P362, 10–13 October 2012.
  • Ram R, Ben-Bassat I, Shpilberg O, Polliack A, Raanani P. The late adverse events of rituximab therapy – rare but there! Leuk. Lymphoma 50(7), 1083–1095 (2009).
  • Kappos L, Leppert D, Tinbergen J, Gerber M, Hauser SL. Risk of infections and malignancies after treatment with anti-CD20 monoclonal antibodies: ocrelizumab and rituximab in rheumatoid arthritis and multiple sclerosis. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P929, 10–13 October 2012.
  • Soelberg Sorensen P, Drulovic J, Havrdova E, Lisby S, Graff O, Shackelford S. Magnetic resonance imaging (MRI) efficacy of ofatumumab in relapsing–remitting multiple sclerosis (RRMS) – 24-week results of a Phase II study. Presented at: 26th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Gothenburg, Sweden, 136, 13–16 October 2010.
  • Brinkman IH, van de Laar MA, Jansen TL, van Roon EN. The potential risk of infections during (prolonged) rituximab therapy in rheumatoid arthritis. Expert Opin. Drug Saf. 10(5), 715–726 (2011).
  • Palazzo E, Yahia SA. Progressive multifocal leukoencephalopathy in autoimmune diseases. Joint Bone Spine 79(4), 351–355 (2012).
  • Polman CH, Reingold SC, Banwell B et al. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann. Neurol. 69(2), 292–302 (2011).
  • Zepp J, Wu L, Li X. IL-17 receptor signaling and T helper 17-mediated autoimmune demyelinating disease. Trends Immunol. 32(5), 232–239 (2011).
  • Ambrosi A, Espinosa A, Wahren-Herlenius M. IL-17: a new actor in IFN-driven systemic autoimmune diseases. Eur. J. Immunol. 42(9), 2274–2284 (2012).
  • Havradová E, Belova A, Goloborodko A et al. Positive proof of concept of AIN457, an antibody against interleukin-17A, in relapsing-remitting multiple sclerosis. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, 168, 10–13 October 2012.
  • Miller AE, O’Connor P, Wolinsky JS et al.; Teriflunomide Multiple Sclerosis Trial Group. Pre-specified subgroup analyses of a placebo-controlled Phase III trial (TEMSO) of oral teriflunomide in relapsing multiple sclerosis. Mult. Scler. 18(11), 1625–1632 (2012).
  • Devonshire V, Havrdova E, Radue EW et al.; FREEDOMS study group. Relapse and disability outcomes in patients with multiple sclerosis treated with fingolimod: subgroup analyses of the double-blind, randomised, placebo-controlled FREEDOMS study. Lancet Neurol. 11(5), 420–428 (2012).
  • Hutchinson M, Kappos L, Calabresi PA et al.; AFFIRM and SENTINEL Investigators. The efficacy of natalizumab in patients with relapsing multiple sclerosis: subgroup analyses of AFFIRM and SENTINEL. J. Neurol. 256(3), 405–415 (2009).
  • Trojano M, Pellegrini F, Paolicelli D et al.; Italian Multiple Sclerosis Database Network Group. Post-marketing of disease modifying drugs in multiple sclerosis: an exploratory analysis of gender effect in interferon β treatment. J. Neurol. Sci. 286(1–2), 109–113 (2009).
  • Ulzheimer JC, Meuth SG, Bittner S, Kleinschnitz C, Kieseier BC, Wiendl H. Therapeutic approaches to multiple sclerosis: an update on failed, interrupted, or inconclusive trials of immunomodulatory treatment strategies. BioDrugs 24(4), 249–274 (2010).
  • Perron H, Garson JA, Bedin F et al. Molecular identification of a novel retrovirus repeatedly isolated from patients with multiple sclerosis. The Collaborative Research Group on Multiple Sclerosis. Proc. Natl Acad. Sci. USA 94(14), 7583–7588 (1997).
  • Ryan FP. Human endogenous retroviruses in multiple sclerosis: potential for novel neuro-pharmacological research. Curr. Neuropharmacol. 9(2), 360–369 (2011).
  • Antony JM, van Marle G, Opii W et al. Human endogenous retrovirus glycoprotein-mediated induction of redox reactants causes oligodendrocyte death and demyelination. Nat. Neurosci. 7(10), 1088–1095 (2004).
  • Firouzi R, Rolland A, Michel M et al. Multiple sclerosis-associated retrovirus particles cause T lymphocyte-dependent death with brain hemorrhage in humanized SCID mice model. J. Neurovirol. 9(1), 79–93 (2003).
  • Curtin F, Lang AB, Perron H et al. Safety and pharmacokinetics of GNbAC1, a humanised monoclonal antibody against the multiple sclerosis retrovirus envelope protein. Presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis. Lyon, France, P558, 10–13 October 2012.
  • Mi S, Lee X, Shao Z et al. LINGO-1 is a component of the Nogo-66 receptor/p75 signaling complex. Nat. Neurosci. 7(3), 221–228 (2004).
  • Lee X, Yang Z, Shao Z et al. NGF regulates the expression of axonal LINGO-1 to inhibit oligodendrocyte differentiation and myelination. J. Neurosci. 27(1), 220–225 (2007).
  • Mi S, Miller RH, Lee X et al. LINGO-1 negatively regulates myelination by oligodendrocytes. Nat. Neurosci. 8(6), 745–751 (2005).
  • Ji B, Li M, Wu WT et al. LINGO-1 antagonist promotes functional recovery and axonal sprouting after spinal cord injury. Mol. Cell. Neurosci. 33(3), 311–320 (2006).
  • Mi S, Hu B, Hahm K et al. LINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis. Nat. Med. 13(10), 1228–1233 (2007).
  • Inoue H, Lin L, Lee X et al. Inhibition of the leucine-rich repeat protein LINGO-1 enhances survival, structure, and function of dopaminergic neurons in Parkinson’s disease models. Proc. Natl Acad. Sci. USA 104(36), 14430–14435 (2007).
  • Lv J, Xu RX, Jiang XD et al. Passive immunization with LINGO-1 polyclonal antiserum afforded neuroprotection and promoted functional recovery in a rat model of spinal cord injury. Neuroimmunomodulation 17(4), 270–278 (2010).
  • Loov C, Fernqvist M, Walmsley A, Marklund N, Erlandsson A. Neutralization of LINGO-1 during in vitro differentiation of neural stem cells results in proliferation of immature neurons. PloS ONE 7(1), e29771 (2012).
  • Tran J, Palaparthy R, Zhao J et al. Safety, tolerability and pharmacokinetics of the anti-LINGO-1 monoclonal antibody BIIB033 in healthy volunteers and subjects with multiple sclerosis. Presented at: 64th American Academy of Neurology Annual Meeting. New Orleans, LA, USA 21–28 April 2012 (P02.021).
  • Gal RL, Vedula SS, Beck R. Corticosteroids for treating optic neuritis. Cochrane Database Syst. Rev. 4, CD001430 (2012).
  • Hamilton JA. Colony-stimulating factors in inflammation and autoimmunity. Nat. Rev. Immunol. 8(7), 533–544 (2008).
  • Tedder TF. CD19: a promising B cell target for rheumatoid arthritis. Nat. Rev. Rheumatol. 5(10), 572–577 (2009).
  • Pelletier D, Hafler DA. Fingolimod for multiple sclerosis. N. Engl. J. Med. 366(4), 339–347 (2012).

Websites

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.