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Review

Treating multiple sclerosis with monoclonal antibodies

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Pages 433-455 | Published online: 10 Jan 2014

References

  • Kleinschmidt-DeMasters BK, Tyler KL. Progressive multifocal leukoencephalopathy complicating treatment with natalizumab and interferon β-1a for multiple sclerosis. N. Engl. J. Med.353(4), 369–374 (2005).
  • 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).
  • 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).
  • Yousry TA, Major EO, Ryschkewitsch C et al. Evaluation of patients treated with natalizumab for progressive multifocal leukoencephalopathy. N. Engl. J. Med.354(9), 924–933 (2006).
  • Panzara MA, Belcher G, Kooijmans M, Kim R, Lynn F, Bozic C. Use of natalizumab in patients with relapsing multiple sclerosis: updated safety results from TOUCH and TYGRIS. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 565, 11–14 October 2007.
  • Compston A, Coles A. Multiple sclerosis. Lancet359(9313), 1221–1231 (2002).
  • Pugliatti M, Rosati G, Carton H et al. The epidemiology of multiple sclerosis in Europe. Eur. J. Neurol.13(7), 700–722 (2006).
  • Frohman EM, Racke MK, Raine CS. Multiple sclerosis – the plaque and its pathogenesis. N. Engl. J. Med.354(9), 942–955 (2006).
  • Ramsaransing GS, De Keyser J. Benign course in multiple sclerosis: a review. Acta Neurol. Scand.113(6), 359–369 (2006).
  • Rovaris M, Confavreux C, Furlan R, Kappos L, Comi G, Filippi M. Secondary progressive multiple sclerosis: current knowledge and future challenges. Lancet Neurol.5(4), 343–354 (2006).
  • Montalban X. Primary progressive multiple sclerosis. Curr. Opin. Neurol.18(3), 261–266 (2005).
  • Thompson AJ, Montalban X, Barkhof F et al. Diagnostic criteria for primary progressive multiple sclerosis: a position paper. Ann. Neurol.47(6), 831–835 (2000).
  • Gayou A, Brochet B, Dousset V. Transitional progressive multiple sclerosis: a clinical and imaging study. J. Neurol. Neurosurg. Psychiatr.63(3), 396–398 (1997).
  • Ingle GT, Stevenson VL, Miller DH et al. Two-year follow-up study of primary and transitional progressive multiple sclerosis. Mult. Scler.8(2), 108–114 (2002).
  • 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).
  • 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).
  • Kohler G, Milstein C. Continuous cultures of fused cells secreting antibody of predefined specificity. Nature256(5517), 495–497 (1975).
  • Kuus-Reichel K, Grauer LS, Karavodin LM, Knott C, Krusemeier M, Kay NE. Will immunogenicity limit the use, efficacy, and future development of therapeutic monoclonal antibodies? Clin. Diagn. Lab. Immunol.1(4), 365–372 (1994).
  • Hohlfeld R, Wekerle H. Drug insight: using monoclonal antibodies to treat multiple sclerosis. Nat. Clin. Pract. Neurol.1(1), 34–44 (2005).
  • Morrison SL, Johnson MJ, Herzenberg LA, Oi VT. Chimeric human antibody molecules: mouse antigen-binding domains with human constant region domains. Proc. Natl Acad. Sci. USA81(21), 6851–6855 (1984).
  • Boulianne GL, Hozumi N, Shulman MJ. Production of functional chimaeric mouse/human antibody. Nature312(5995), 643–646 (1984).
  • Jones PT, Dear PH, Foote J, Neuberger MS, Winter G. Replacing the complementarity-determining regions in a human antibody with those from a mouse. Nature321(6069), 522–525 (1986).
  • Lofgren JA, Dhandapani S, Pennucci JJ et al. Comparing ELISA and surface plasmon resonance for assessing clinical immunogenicity of panitumumab. J. Immunol.178(11), 7467–7472 (2007).
  • MacDonald JK, McDonald JW. Natalizumab for induction of remission in Crohn’s disease. Cochrane Database Syst. Rev.1, CD006097 (2007).
  • Targan SR, Feagan BG, Fedorak RN et al. Natalizumab for the treatment of active Crohn’s disease: results of the ENCORE Trial. Gastroenterology132(5), 1672–1683 (2007).
  • Traynor K. FDA advisers endorse natalizumab for Crohn’s disease. Am. J. Health Syst. Pharm.64(18), 1886–1890 (2007).
  • Bochner BS, Luscinskas FW, Gimbrone MA Jr et al. Adhesion of human basophils, eosinophils, and neutrophils to interleukin 1-activated human vascular endothelial cells: contributions of endothelial cell adhesion molecules. J. Exp. Med.173(6), 1553–1557 (1991).
  • Alon R, Kassner PD, Carr MW, Finger EB, Hemler ME, Springer TA. The integrin VLA-4 supports tethering and rolling in flow on VCAM-1. J. Cell Biol.128(6), 1243–1253 (1995).
  • Johnston B, Kubes P. The α4-integrin: an alternative pathway for neutrophil recruitment? Immunol. Today20(12), 545–550 (1999).
  • Fleming SD, Anderson J, Wilson F, Shea-Donohue T, Tsokos GC. C5 is required for CD49d expression on neutrophils and VCAM expression on vascular endothelial cells following mesenteric ischemia/reperfusion. Clin. Immunol.106(1), 55–64 (2003).
  • Arroyo AG, Yang JT, Rayburn H, Hynes RO. Differential requirements for α4 integrins during fetal and adult hematopoiesis. Cell85(7), 997–1008 (1996).
  • Arroyo AG, Yang JT, Rayburn H, Hynes RO. α4 integrins regulate the proliferation/differentiation balance of multilineage hematopoietic progenitors in vivo.Immunity11(5), 555–566 (1999).
  • Wayner EA, Garcia-Pardo A, Humphries MJ, McDonald JA, Carter WG. Identification and characterization of the T lymphocyte adhesion receptor for an alternative cell attachment domain (CS-1) in plasma fibronectin. J. Cell Biol.109(3), 1321–1330 (1989).
  • Bayless KJ, Meininger GA, Scholtz JM, Davis GE. Osteopontin is a ligand for the α4β1 integrin. J. Cell. Sci.111(Pt 9), 1165–1174 (1998).
  • Bayless KJ, Davis GE. Identification of dual α 4β1 integrin binding sites within a 38 amino acid domain in the N-terminal thrombin fragment of human osteopontin. J. Biol. Chem.276(16), 13483–13489 (2001).
  • Briskin M, Winsor-Hines D, Shyjan A et al. Human mucosal addressin cell adhesion molecule-1 is preferentially expressed in intestinal tract and associated lymphoid tissue. Am. J. Pathol.151(1), 97–110 (1997).
  • Streeter PR, Berg EL, Rouse BT, Bargatze RF, Butcher EC. A tissue-specific endothelial cell molecule involved in lymphocyte homing. Nature331(6151), 41–46 (1988).
  • Berlin C, Berg EL, Briskin MJ et al. a4 b7 integrin mediates lymphocyte binding to the mucosal vascular addressin MAdCAM-1. Cell74(1), 185–195 (1993).
  • Han J, Liu S, Rose DM, Schlaepfer DD, McDonald H, Ginsberg MH. Phosphorylation of the integrin a4 cytoplasmic domain regulates paxillin binding. J. Biol. Chem.276(44), 40903–40909 (2001).
  • Goldfinger LE, Han J, Kiosses WB, Howe AK, Ginsberg MH. Spatial restriction of α4 integrin phosphorylation regulates lamellipodial stability and α4β1-dependent cell migration. J. Cell Biol.162(4), 731–741 (2003).
  • Alon R, Feigelson SW, Manevich E et al. α4β1-dependent adhesion strengthening under mechanical strain is regulated by paxillin association with the α4-cytoplasmic domain. J. Cell Biol.171(6), 1073–1084 (2005).
  • Rose DM, Liu S, Woodside DG, Han J, Schlaepfer DD, Ginsberg MH. Paxillin binding to the α 4 integrin subunit stimulates LFA-1 (integrin α L β 2)-dependent T cell migration by augmenting the activation of focal adhesion kinase/proline-rich tyrosine kinase-2. J. Immunol.170(12), 5912–5918 (2003).
  • Han J, Rose DM, Woodside DG, Goldfinger LE, Ginsberg MH. Integrin α 4 β 1-dependent T cell migration requires both phosphorylation and dephosphorylation of the α 4 cytoplasmic domain to regulate the reversible binding of paxillin. J. Biol. Chem.278(37), 34845–34853 (2003).
  • Nishiya N, Kiosses WB, Han J, Ginsberg MH. An α4 integrin-paxillin-Arf-GAP complex restricts Rac activation to the leading edge of migrating cells. Nat. Cell Biol.7(4), 343–352 (2005).
  • Vitale N, Patton WA, Moss J, Vaughan M, Lefkowitz RJ, Premont RT. GIT proteins, a novel family of phosphatidylinositol 3,4, 5-trisphosphate-stimulated GTPase-activating proteins for ARF6. J. Biol. Chem.275(18), 13901–13906 (2000).
  • Rose DM, Alon R, Ginsberg MH. Integrin modulation and signaling in leukocyte adhesion and migration. Immunol. Rev.218, 126–134 (2007).
  • Steinman L. Blocking adhesion molecules as therapy for multiple sclerosis: natalizumab. Nat. Rev. Drug Discov.4(6), 510–518 (2005).
  • Niino M, Bodner C, Simard ML et al. Natalizumab effects on immune cell responses in multiple sclerosis. Ann. Neurol.59(5), 748–754 (2006).
  • Stuve 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).
  • Stenner MP, Waschbisch A, Buck D, Einsele H, Toyka KV, Wiendl H. Effect of natalizumab on regulatory T-cells: analysis of frequency, migratory behaviour and suppressive capacity of two natural Treg populations in vitro and ex vivo. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 560, 11–14 October 2007.
  • Toutzaris D, Zohren F, Haas R, Hartung H-P, Kieseier BC. Natalizumab increases the number of circulating CD34+ cells in the peripheral venous blood of multiple sclerosis patients. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 568, 11–14 October 2007.
  • Podolsky DK. Selective adhesion-molecule therapy and inflammatory bowel disease – a tale of Janus? N. Engl. J. Med.353(18), 1965–1968 (2005).
  • Rudick RA, Sandrock A. Natalizumab: α 4-integrin antagonist selective adhesion molecule inhibitors for MS. Expert Rev. Neurotherapeutics4(4), 571–580 (2004).
  • Kachuck NJ. Challenges and opportunities: what we are learning from the clinical natalizumab experience. Expert Rev. Neurotherapeutics5(5), 605–615 (2005).
  • Miller DH, Soon D, Fernando KT et al. MRI outcomes in a placebo-controlled trial of natalizumab in relapsing MS. Neurology68(17), 1390–1401 (2007).
  • Polman CH, O’Connor PW, Havrdova E et al. A randomized, placebo-controlled trial of natalizumab for relapsing multiple sclerosis. N. Engl. J. Med.354(9), 899–910 (2006).
  • Rudick RA, Stuart WH, Calabresi PA et al. Natalizumab plus interferon β-1a for relapsing multiple sclerosis. N. Engl. J. Med.354(9), 911–923 (2006).
  • O’Connor PW, Goodman A, Kappos L et al. The efficacy of natalizumab monotherapy over 3 years of treatment in patients with relapsing multiple sclerosis. Presented at: 59th Annual Meeting of the American Academy of Neurology. Boston, MA, USA, P06.082, 28 April–5 May 2007.
  • Rudick RA, Miller D, Hass S et al. Health-related quality of life in multiple sclerosis: effects of natalizumab. Ann. Neurol.62(4), 335–346 (2007).
  • Krumbholz M, Pellkofer H, Gold R, Hoffmann LA, Hohlfeld R, Kumpfel T. Delayed allergic reaction to natalizumab associated with early formation of neutralizing antibodies. Arch. Neurol.64(9), 1331–1333 (2007).
  • Astrom KE, Mancall EL, Richardson EP Jr. Progressive multifocal leuko-encephalopathy; a hitherto unrecognized complication of chronic lymphatic leukaemia and Hodgkin’s disease. Brain81(1), 93–111 (1958).
  • Padgett BL, Walker DL, ZuRhein GM, Eckroade RJ, Dessel BH. Cultivation of papova-like virus from human brain with progressive multifocal leucoencephalopathy. Lancet1(7712), 1257–1260 (1971).
  • Knowles WA, Pipkin P, Andrews N et al. Population-based study of antibody to the human polyomaviruses BKV and JCV and the simian polyomavirus SV40. J. Med. Virol.71(1), 115–123 (2003).
  • Arthur RR, Shah KV. Occurrence and significance of papovaviruses BK and JC in the urine. Prog. Med. Virol.36, 42–61 (1989).
  • Arthur RR, Shah KV, Charache P, Saral R. BK and JC virus infections in recipients of bone marrow transplants. J. Infect. Dis.158(3), 563–569 (1988).
  • Berger JR, Concha M. Progressive multifocal leukoencephalopathy: the evolution of a disease once considered rare. J. Neurovirol.1(1), 5–18 (1995).
  • Ransohoff RM. Natalizumab and PML. Nat. Neurosci.8(10), 1275 (2005).
  • Khalili K, White MK, Lublin F, Ferrante P, Berger JR. Reactivation of JC virus and development of PML in patients with multiple sclerosis. Neurology68(13), 985–990 (2007).
  • Kappos L, Bates D, Hartung HP et al. Natalizumab treatment for multiple sclerosis: recommendations for patient selection and monitoring. Lancet Neurol.6(5), 431–441 (2007).
  • Stuve O, Marra CM, Cravens PD et al. Potential risk of progressive multifocal leukoencephalopathy with natalizumab therapy: possible interventions. Arch. Neurol.64(2), 169–176 (2007).
  • Khatri B, Fox R, Koo A et al. The effect of plasma exchange in accelerating clearance of natalizumab in patients with multiple sclerosis: results of the PLEX study. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 576, 11–14 October 2007.
  • Bozic C, Belcher G, Koojimans M, Kim R, Lynn F, Panzara M. The Safety of Natalizumab in Patients with Relapsing Multiple Sclerosis: An Update from TOUCH and TYGRIS. Presented at: 59th Annual Meeting of the American Academy of Neurology. Boston, MA, USA, P06.095, 28 April–5 May 2007.
  • O’Connor P, Goodman A, Kappos L et al. Safety of natalizumab upon re-dosing: preliminary results from the STRATA study. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 564, 11–14 October 2007.
  • Noronha A. Neutralizing antibodies to interferon. Neurology68(24 Suppl. 4), S16–S22 (2007).
  • Schellekens H. Bioequivalence and the immunogenicity of biopharmaceuticals. Nat. Rev. Drug Discov.1(6), 457–462 (2002).
  • Calabresi PA, Giovannoni G, Confavreux C et al. The incidence and significance of anti-natalizumab antibodies: results from AFFIRM and SENTINEL. Neurology69(14), 1391–1403 (2007).
  • Vellinga MM, Castelijns JA, Barkhof F, Uitdehaag BM, Polman CH. Postwithdrawal rebound increase in T2 lesional activity in natalizumab-treated MS patients. Neurology PMID: 17872364 (2007) (Epub ahead of print).
  • Alinari L, Lapalombella R, Andritsos L, Baiocchi RA, Lin TS, Byrd JC. Alemtuzumab (Campath-1H) in the treatment of chronic lymphocytic leukemia. Oncogene26(25), 3644–3653 (2007).
  • Hillmen P, Skotnicki A, Robak T. Alemtuzumab compared with chlorambucil as first line therapy for patients requiring treatment for chronic lymphocytic leukemia. J. Clin. Oncol.25(35), 5616–5623 (2007).
  • Reiff A. A review of Campath in autoimmune disease: biologic therapy in the gray zone between immunosuppression and immunoablation. Hematology10(2), 79–93 (2005).
  • Morris PJ, Russell NK. Alemtuzumab (Campath-1H): a systematic review in organ transplantation. Transplantation81(10), 1361–1367 (2006).
  • Kirk AD, Hale DA, Mannon RB et al. Results from a human renal allograft tolerance trial evaluating the humanized CD52-specific monoclonal antibody alemtuzumab (CAMPATH-1H). Transplantation76(1), 120–129 (2003).
  • Hasegawa A, Fu Y, Tsubamoto H et al. Epitope analysis for human sperm-immobilizing monoclonal antibodies, MAb H6–3C4, 1G12 and campath-1. Mol. Hum. Reprod.9(6), 337–343 (2003).
  • Domagala A, Kurpisz M. CD52 antigen – a review. Med. Sci. Monit.7(2), 325–331 (2001).
  • Cox AL, Thompson SA, Jones JL et al. Lymphocyte homeostasis following therapeutic lymphocyte depletion in multiple sclerosis. Eur. J. Immunol.35(11), 3332–3342 (2005).
  • Watanabe T, Masuyama J, Sohma Y et al. CD52 is a novel costimulatory molecule for induction of CD4+ regulatory T cells. Clin. Immunol.120(3), 247–259 (2006).
  • Viglietta V, Baecher-Allan C, Weiner HL, Hafler DA. Loss of functional suppression by CD4+CD25+ regulatory T cells in patients with multiple sclerosis. J. Exp. Med.199(7), 971–979 (2004).
  • Moreau T, Coles A, Wing M et al. Transient increase in symptoms associated with cytokine release in patients with multiple sclerosis. Brain119(Pt 1), 225–237 (1996).
  • Hale G, Bright S, Chumbley G et al. Removal of T cells from bone marrow for transplantation: a monoclonal antilymphocyte antibody that fixes human complement. Blood62(4), 873–882 (1983).
  • Heit W, Bunjes D, Wiesneth M et al. Ex vivo T-cell depletion with the monoclonal antibody Campath-1 plus human complement effectively prevents acute graft-versus-host disease in allogeneic bone marrow transplantation. Br. J. Haematol.64(3), 479–486 (1986).
  • Dyer MJ, Hale G, Hayhoe FG, Waldmann H. Effects of CAMPATH-1 antibodies in vivo in patients with lymphoid malignancies: influence of antibody isotype. Blood73(6), 1431–1439 (1989).
  • Mould DR, Baumann A, Kuhlmann J et al. Population pharmacokinetics-pharmacodynamics of alemtuzumab (Campath) in patients with chronic lymphocytic leukaemia and its link to treatment response. Br. J. Clin. Pharmacol.64(3), 278–291 (2007).
  • Morris EC, Rebello P, Thomson KJ et al. Pharmacokinetics of alemtuzumab used for in vivo and in vitro T-cell depletion in allogeneic transplantations: relevance for early adoptive immunotherapy and infectious complications. Blood102(1), 404–406 (2003).
  • Hale G, Rebello P, Brettman LR et al. Blood concentrations of alemtuzumab and antiglobulin responses in patients with chronic lymphocytic leukemia following intravenous or subcutaneous routes of administration. Blood104(4), 948–955 (2004).
  • Isaacs JD, Watts RA, Hazleman BL et al. Humanised monoclonal antibody therapy for rheumatoid arthritis. Lancet340(8822), 748–752 (1992).
  • 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).
  • Moreau T, Thorpe J, Miller D et al. Preliminary evidence from magnetic resonance imaging for reduction in disease activity after lymphocyte depletion in multiple sclerosis. Lancet344(8918), 298–301 (1994).
  • Coles AJ, Wing MG, Molyneux P et al. Monoclonal antibody treatment exposes three mechanisms underlying the clinical course of multiple sclerosis. Ann. Neurol.46(3), 296–304 (1999).
  • Coles AJ, Wing M, Smith S et al. Pulsed monoclonal antibody treatment and autoimmune thyroid disease in multiple sclerosis. Lancet354(9191), 1691–1695 (1999).
  • Fox E, Mayer L, Sullivan H et al. Two-year results with alemtuzumab in patients with active relapsing–remitting multiple sclerosis who have failed licensed β interferon therapies. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 568, 11–14 October 2007.
  • Coles A. Efficacy of alemtuzumab in relapsing–remitting multiple sclerosis is independent of baseline status. Presented at: 17th Meeting of the European Neurological Society. Rhodes, Greece, 16–20 June 2007.
  • Sullivan H, Group TCS. ITP following treatment of multiple sclerosis patients with alemtuzumab in CAMMS223: case reports and risk management plan implementation. Presented at: 59th American Academy of Neurology Annual Meeting. S32.004. Boston, MA, USA, 28 April–5 May (2007).
  • Coles A, Group TCS. Two-year interim analysis of thyroid abnormalities in a trial of alemtuzumab vs. high-dose interferon β-1a for treatment of relapsing–remitting multiple sclerosis. Presented at: 59th American Academy of Neurology Annual Meeting. P06.087. Boston, MA, USA, 28 April–5 May 2007.
  • Fox EJ, Coles A, Margolin DH et al. ITP following treatment of multiple sclerosis patients with alemtuzumab in CAMMS223: case reports and risk management plan implementation. Presented at: 22nd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Madrid, Spain, 27 April–30 April 2006.
  • Coles AJ, Group TCIS. Alemtuzumab improved multiple sclerosis functional composite scores and delayed time to first relapse at 2-year interim analysis compared to subcutaneous interferon β-1a. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 557, 11–14 October 2007.
  • Reff ME, Carner K, Chambers KS et al. Depletion of B cells in vivo by a chimeric mouse human monoclonal antibody to CD20. Blood83(2), 435–445 (1994).
  • Cvetkovic RS, Perry CM. Rituximab: a review of its use in non-Hodgkin’s lymphoma and chronic lymphocytic leukaemia. Drugs66(6), 791–820 (2006).
  • Edwards JC, Szczepanski L, Szechinski J et al. Efficacy of B-cell-targeted therapy with rituximab in patients with rheumatoid arthritis. N. Engl. J. Med.350(25), 2572–2581 (2004).
  • Cohen SB, Emery P, Greenwald MW et al. Rituximab for rheumatoid arthritis refractory to anti-tumor necrosis factor therapy: results of a multicenter, randomized, double-blind, placebo-controlled, Phase III trial evaluating primary efficacy and safety at twenty-four weeks. Arthritis Rheum.54(9), 2793–2806 (2006).
  • Edwards JC, Cambridge G. B-cell targeting in rheumatoid arthritis and other autoimmune diseases. Nat. Rev. Immunol.6(5), 394–403 (2006).
  • Capobianco M, Malucchi S, di Sapio A et al. Variable responses to rituximab treatment in neuromyelitis optica (Devic’s disease). Neurol. Sci.28(4), 209–211 (2007).
  • Cree BA, Lamb S, Morgan K, Chen A, Waubant E, Genain C. An open label study of the effects of rituximab in neuromyelitis optica. Neurology64(7), 1270–1272 (2005).
  • Genain C, Isla J, Gardell J et al. T-cell suppression following treatment with rituximab in neuromyelitis optica. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 551, 11–14 October 2007.
  • Nadler LM, Ritz J, Hardy R, Pesando JM, Schlossman SF, Stashenko P. A unique cell surface antigen identifying lymphoid malignancies of B cell origin. J. Clin. Invest.67(1), 134–140 (1981).
  • Rieckmann P, Wilson GL, Thevenin C, Hong JX, Kehrl JH. Analysis of cis-acting elements present in the CD20/B1 antigen promoter. J. Immunol.147(11), 3994–3999 (1991).
  • Tedder TF, Engel P. CD20: a regulator of cell-cycle progression of B lymphocytes. Immunol. Today15(9), 450–454 (1994).
  • Cragg MS, Walshe CA, Ivanov AO, Glennie MJ. The biology of CD20 and its potential as a target for mAb therapy. Curr. Dir. Autoimmun.8, 140–174 (2005).
  • Maloney DG, Liles TM, Czerwinski DK et al. Phase I clinical trial using escalating single-dose infusion of chimeric anti-CD20 monoclonal antibody (IDEC-C2B8) in patients with recurrent B-cell lymphoma. Blood84(8), 2457–2466 (1994).
  • Glennie MJ, French RR, Cragg MS, Taylor RP. Mechanisms of killing by anti-CD20 monoclonal antibodies. Mol. Immunol.44(16), 3823–3837 (2007).
  • Wu J, Edberg JC, Redecha PB et al. A novel polymorphism of FcgammaRIIIa (CD16) alters receptor function and predisposes to autoimmune disease. J. Clin. Invest.100(5), 1059–1070 (1997).
  • Koene HR, Kleijer M, Algra J, Roos D, von dem Borne AE, de Haas M. FcγRIIIa-158V/F polymorphism influences the binding of IgG by natural killer cell FcγRIIIa, independently of the FcγRIIIa-48L/R/H phenotype. Blood90(3), 1109–1114 (1997).
  • Cartron G, Dacheux L, Salles G et al. Therapeutic activity of humanized anti-CD20 monoclonal antibody and polymorphism in IgG Fc receptor FcgRIIIa gene. Blood99(3), 754–758 (2002).
  • Anolik JH, Campbell D, Felgar RE et al. The relationship of FcγRIIIa genotype to degree of B cell depletion by rituximab in the treatment of systemic lupus erythematosus. Arthritis Rheum.48(2), 455–459 (2003).
  • Di Gaetano N, Cittera E, Nota R et al. Complement activation determines the therapeutic activity of rituximab in vivo. J. Immunol.171(3), 1581–1587 (2003).
  • Golay J, Lazzari M, Facchinetti V et al. CD20 levels determine the in vitro susceptibility to rituximab and complement of B-cell chronic lymphocytic leukemia: further regulation by CD55 and CD59. Blood98(12), 3383–3389 (2001).
  • Golay J, Zaffaroni L, Vaccari T et al. Biologic response of B lymphoma cells to anti-CD20 monoclonal antibody rituximab in vitro: CD55 and CD59 regulate complement-mediated cell lysis. Blood95(12), 3900–3908 (2000).
  • Bellosillo B, Villamor N, Lopez-Guillermo A et al. Complement-mediated cell death induced by rituximab in B-cell lymphoproliferative disorders is mediated in vitro by a caspase-independent mechanism involving the generation of reactive oxygen species. Blood98(9), 2771–2777 (2001).
  • Weng WK, Levy R. Expression of complement inhibitors CD46, CD55, and CD59 on tumor cells does not predict clinical outcome after rituximab treatment in follicular non-Hodgkin lymphoma. Blood98(5), 1352–1357 (2001).
  • Tedder TF, Forsgren A, Boyd AW, Nadler LM, Schlossman SF. Antibodies reactive with the B1 molecule inhibit cell cycle progression but not activation of human B lymphocytes. Eur. J. Immunol.16(8), 881–887 (1986).
  • Golay JT, Clark EA, Beverley PC. The CD20 (Bp35) antigen is involved in activation of B cells from the G0 to the G1 phase of the cell cycle. J. Immunol.135(6), 3795–3801 (1985).
  • Byrd JC, Kitada S, Flinn IW et al. The mechanism of tumor cell clearance by rituximab in vivo in patients with B-cell chronic lymphocytic leukemia: evidence of caspase activation and apoptosis induction. Blood99(3), 1038–1043 (2002).
  • Shan D, Ledbetter JA, Press OW. Signaling events involved in anti-CD20-induced apoptosis of malignant human B cells. Cancer Immunol. Immunother.48(12), 673–683 (2000).
  • Hofmeister JK, Cooney D, Coggeshall KM. Clustered CD20 induced apoptosis: src-family kinase, the proximal regulator of tyrosine phosphorylation, calcium influx, and caspase 3-dependent apoptosis. Blood Cells Mol. Dis.26(2), 133–143 (2000).
  • Cartron G, Blasco H, Paintaud G, Watier H, Le Guellec C. Pharmacokinetics of rituximab and its clinical use: thought for the best use? Crit. Rev. Oncol. Hematol.62(1), 43–52 (2007).
  • Ng CM, Bruno R, Combs D, Davies B. Population pharmacokinetics of rituximab (anti-CD20 monoclonal antibody) in rheumatoid arthritis patients during a Phase II clinical trial. J. Clin. Pharmacol.45(7), 792–801 (2005).
  • Breedveld F, Agarwal S, Yin M et al. Rituximab pharmacokinetics in patients with rheumatoid arthritis: B-cell levels do not correlate with clinical response. J. Clin. Pharmacol.47(9), 1119–1128 (2007).
  • Bar-Or A, Calabresi P, Arnold DL et al. Safety, pharmacodynamics, and activity of rituximab in patients with relapsing–remitting multiple sclerosis: a Phase I, multicentre, open-label clinical trial. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, page 555, 11–14 October 2007.
  • Monson NL, Cravens PD, Frohman EM, Hawker K, Racke MK. Effect of rituximab on the peripheral blood and cerebrospinal fluid B cells in patients with primary progressive multiple sclerosis. Arch. Neurol.62(2), 258–264 (2005).
  • Petereit HF, Rubbert A. Effective suppression of cerebrospinal fluid B cells by rituximab and cyclophosphamide in progressive multiple sclerosis. Arch. Neurol.62(10), 1641–1642; author reply 1642 (2005).
  • Stuve O, Cepok S, Elias B et al. Clinical stabilization and effective B-lymphocyte depletion in the cerebrospinal fluid and peripheral blood of a patient with fulminant relapsing–remitting multiple sclerosis. Arch. Neurol.62(10), 1620–1623 (2005).
  • Cross AH, Stark JL, Lauber J, Ramsbottom MJ, Lyons JA. Rituximab reduces B cells and T cells in cerebrospinal fluid of multiple sclerosis patients. J. Neuroimmunol.180(1–2), 63–70 (2006).
  • Cross AH, Trotter JL, Lyons J. B cells and antibodies in CNS demyelinating disease. J. Neuroimmunol.112(1–2), 1–14 (2001).
  • Waubant E, Hauser S, Arnold DL et al. Safety and efficacy of rituximab in adults with relapsing–remitting multiple sclerosis: results of a Phase II placebo-controlled, multicentre trial through 48 weeks. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 554, 11–14 October 2007.
  • Hawker K, Freedman MS, O’Connor P et al. Rituximab in patients with primary progressive multiple sclerosis: demographics in a Phase II/III randomised, double-blind, placebo-controlled multicentre trial. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 553, 11–14 October 2007.
  • Calabrese LH, Molloy ES, Huang D, Ransohoff RM. Progressive multifocal leukoencephalopathy in rheumatic diseases: evolving clinical and pathologic patterns of disease. Arthritis Rheum.56(7), 2116–2128 (2007).
  • Lassmann H, Bruck W, Lucchinetti CF. The immunopathology of multiple sclerosis: an overview. Brain Pathol.17(2), 210–218 (2007).
  • Keegan M, Konig F, McClelland R et al. Relation between humoral pathological changes in multiple sclerosis and response to therapeutic plasma exchange. Lancet366(9485), 579–582 (2005).
  • Queen C, Schneider WP, Selick HE et al. A humanized antibody that binds to the interleukin 2 receptor. Proc. Natl Acad. Sci. USA86(24), 10029–10033 (1989).
  • Uchiyama T, Broder S, Waldmann TA. A monoclonal antibody (anti-Tac) reactive with activated and functionally mature human T cells. I. Production of anti-Tac monoclonal antibody and distribution of Tac (+) cells. J. Immunol.126(4), 1393–1397 (1981).
  • Uchiyama T, Nelson DL, Fleisher TA, Waldmann TA. A monoclonal antibody (anti-Tac) reactive with activated and functionally mature human T cells. II. Expression of Tac antigen on activated cytotoxic killer T cells, suppressor cells, and on one of two types of helper T cells. J. Immunol.126(4), 1398–1403 (1981).
  • Sandrini S. Use of IL-2 receptor antagonists to reduce delayed graft function following renal transplantation: a review. Clin. Transplant.19(6), 705–710 (2005).
  • Waldmann TA. Anti-Tac (daclizumab, Zenapax) in the treatment of leukemia, autoimmune diseases, and in the prevention of allograft rejection: a 25-year personal odyssey. J. Clin. Immunol.27(1), 1–18 (2007).
  • Korsmeyer SJ, Greene WC, Cossman J et al. Rearrangement and expression of immunoglobulin genes and expression of Tac antigen in hairy cell leukemia. Proc. Natl Acad. Sci. USA80(14), 4522–4526 (1983).
  • Holter W, Goldman CK, Casabo L, Nelson DL, Greene WC, Waldmann TA. Expression of functional IL 2 receptors by lipopolysaccharide and interferon-γ stimulated human monocytes. J. Immunol.138(9), 2917–2922 (1987).
  • Sakaguchi S. Naturally arising CD4+ regulatory t cells for immunologic self-tolerance and negative control of immune responses. Annu. Rev. Immunol.22, 531–562 (2004).
  • Cooper MA, Fehniger TA, Turner SC et al. Human natural killer cells: a unique innate immunoregulatory role for the CD56(bright) subset. Blood97(10), 3146–3151 (2001).
  • International Multiple Sclerosis Genetics Consortium, Hafler DA, Compston A et al. Risk alleles for multiple sclerosis identified by a genomewide study. N. Engl. J. Med.357(9), 927–929 (2007).
  • Abbas AK, Murphy KM, Sher A. Functional diversity of helper T lymphocytes. Nature383(6603), 787–793 (1996).
  • Crane IJ, Forrester JV. Th1 and Th2 lymphocytes in autoimmune disease. Crit. Rev. Immunol.25(2), 75–102 (2005).
  • Umetsu DT, McIntire JJ, Akbari O, Macaubas C, DeKruyff RH. Asthma: an epidemic of dysregulated immunity. Nat. Immunol.3(8), 715–720 (2002).
  • Kikly K, Liu L, Na S, Sedgwick JD. The IL-23/Th(17) axis: therapeutic targets for autoimmune inflammation. Curr. Opin. Immunol.18(6), 670–675 (2006).
  • Sakaguchi S, Ono M, Setoguchi R et al. Foxp3+ CD25+ CD4+ natural regulatory T cells in dominant self-tolerance and autoimmune disease. Immunol. Rev.212, 8–27 (2006).
  • Laurence A, Tato CM, Davidson TS et al. Interleukin-2 signaling via STAT5 constrains T helper 17 cell generation. Immunity26(3), 371–381 (2007).
  • Sharon M, Klausner RD, Cullen BR, Chizzonite R, Leonard WJ. Novel interleukin-2 receptor subunit detected by cross-linking under high-affinity conditions. Science234(4778), 859–863 (1986).
  • Sugamura K, Asao H, Kondo M et al. The interleukin-2 receptor γ chain: its role in the multiple cytokine receptor complexes and T cell development in XSCID. Annu. Rev. Immunol.14, 179–205 (1996).
  • Tkaczuk J, Yu CL, Baksh S et al. Effect of anti-IL-2Rα antibody on IL-2-induced Jak/STAT signaling. Am. J. Transplant.2(1), 31–40 (2002).
  • 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. USA103(15), 5941–5946 (2006).
  • Zhang B, Yamamura T, Kondo T, Fujiwara M, Tabira T. Regulation of experimental autoimmune encephalomyelitis by natural killer (NK) cells. J. Exp. Med.186(10), 1677–1687 (1997).
  • Willerford DM, Chen J, Ferry JA, Davidson L, Ma A, Alt FW. Interleukin-2 receptor a chain regulates the size and content of the peripheral lymphoid compartment. Immunity3(4), 521–530 (1995).
  • Wakabayashi K, Lian ZX, Moritoki Y et al. IL-2 receptor α(-/-) mice and the development of primary biliary cirrhosis. Hepatology44(5), 1240–1249 (2006).
  • Roifman CM. Human IL-2 receptor a chain deficiency. Pediatr. Res.48(1), 6–11 (2000).
  • Caudy AA, Reddy ST, Chatila T, Atkinson JP, Verbsky JW. CD25 deficiency causes an immune dysregulation, polyendocrinopathy, enteropathy, X-linked-like syndrome, and defective IL-10 expression from CD4 lymphocytes. J. Allergy Clin. Immunol.119(2), 482–487 (2007).
  • Aoki CA, Roifman CM, Lian ZX et al. IL-2 receptor α deficiency and features of primary biliary cirrhosis. J. Autoimmun.27(1), 50–53 (2006).
  • Snyder JT, Shen J, Azmi H et al. Direct inhibition of CD40L expression can contribute to the clinical efficacy of daclizumab independently of its effects on cell division and Th1/Th2 cytokine production. Blood109(12), 5399–5406 (2007).
  • No authors listed. TNF neutralization in MS: results of a randomized, placebo-controlled multicenter study. The Lenercept Multiple Sclerosis Study Group and The University of British Columbia MS/MRI Analysis Group. Neurology53(3), 457–465 (1999).
  • Vincenti F, Kirkman R, Light S et al. Interleukin-2-receptor blockade with daclizumab to prevent acute rejection in renal transplantation. Daclizumab Triple Therapy Study Group. N. Engl. J. Med.338(3), 161–165 (1998).
  • Webster AC, Playford EG, Higgins G, Chapman JR, Craig J. Interleukin 2 receptor antagonists for kidney transplant recipients. Cochrane Database Syst. Rev. (Online), CD003897 (2004).
  • Nashan B, Light S, Hardie IR, Lin A, Johnson JR. Reduction of acute renal allograft rejection by daclizumab. Daclizumab Double Therapy Study Group. Transplantation67(1), 110–115 (1999).
  • Bielekova B, Richert N, Howard T et al. Humanized anti-CD25 (daclizumab) inhibits disease activity in multiple sclerosis patients failing to respond to interferon β. Proc. Natl Acad. Sci. USA101(23), 8705–8708 (2004).
  • Rose JW, Watt HE, White AT, Carlson NG. Treatment of multiple sclerosis with an anti-interleukin-2 receptor monoclonal antibody. Ann. Neurol.56(6), 864–867 (2004).
  • Rose JW, Burns JB, Bjorklund J, Klein J, Watt HE, Carlson NG. Daclizumab Phase II trial in relapsing and remitting multiple sclerosis: MRI and clinical results. Neurology69(8), 785–789 (2007).
  • Ali EN, Stazzone LA, Brown BA, Weiner H, Khoury S. Daclizumab in the treatment of patients with multiple sclerosis. Presented at: 59th Annual Meeting of the American Academy of Neurology. 02.005. Boston, MA, USA, 28 April–5 May (2007).
  • Montalban X, Wynn D, Kaufman M, Wang M, Fong A. Preliminary CHOICE results: a Phase 2, randomised, double-blind, placebo-controlled multicentre study of subcutaneous daclixumab in patients with active, relapsing forms of multiple sclerosis on interferon B. Presented at: 23rd Congress of the European Committee for the Treatment and Research in Multiple Sclerosis. Prague, Czech Republic, 50 11–14 October 2007.
  • Kieseier BC, Wiendl H. Oral disease-modifying treatments for multiple sclerosis: the story so far. CNS drugs21(6), 483–502 (2007).

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