Page 81 - XXIV Monografías en Esclerosis Múltiple

MECANISMOS DE ACCIÓN DE LOS FÁRMACOS DE ALTA EFICACIA
03
BIBLIOGRAFÍA
1. Compston A, Coles A. Multiple sclerosis. Lancet. 2002;359:1221-31.
2. Ingwersen J, Aktas O, Kuery P, Kieseier B, Boyko A, Hartung HP. Fingolimod in multiple sclerosis:
mechanisms of action and clinical efficacy. Clin Immunol. 2012;142:15-24.
3. Takabe K, Paugh SW, Milstien S, Spiegel S. “Inside-out” signaling of sphingosine-1-phosphate:
therapeutic targets. Pharmacol Rev. 2008;60:181-95.
4. Mehling M, Brinkmann V, Antel J, Bar-Or A, Goebels N, Vedrine C, et al. FTY720 therapy exerts
differential effects on T cell subsets in multiple sclerosis. Neurology. 2008;71:1261-7.
5. Pitteri M, Magliozzi R, Bajrami A, Camera V, Calabrese M. Potential neuroprotective effect of fingolimod
in multiple sclerosis and its association with clinical variables. Expert Opin Pharmacother. 2018;3:1-9. 6. Horga A, Horga de la Parte JF. Natalizumab en el tratamiento de la esclerosis múltiple. Rev Neurol.
2007;45:293-303.
7. Rice GPA, Hartung HP, Calabresi PA. Anti-a4 integrin therapy for multiple sclerosis. Mechanisms
and rationale. Neurology. 2005;64:1336-42.
8. Rudick RA, Sandrock A. Natalizumab: alpha 4-integrin antagonist selective adhesion molecule
inhibitors for MS. Expert Rev Neurother. 2004;4:571-80.
9. Balasa RI, Simu M, Voidazan S, Barcutean LI, Bajko Z, Hutanu A, et al. Natalizumab Changes
the Peripheral Profile of the Th17 Panel in MS Patients:New Mechanisms of Action. CNS Neurol
Disord Drug Targets. 2017;16:1018-26.
10. Warnke C, Stettner M, Lehmensiek V, Dehmel T, Mausberg AK, von Geldern G, et al. Natali-
zumab exerts a suppressive effect on surrogates of B cell function in blood and CSF. Mult Scler.
2015;21:1036-44.
11. Segal BM, Stuve O. Primary progressive multiple sclerosis: why we are failing. Lancet.
2016;387:1032-4.
12. Villar LM, Costa-Frossard L, Masterman T, Fernández O, Montalbán X, Casanova B, et al. Lip-
id-specific immunoglobulin M bands in cerebrospinal fluid are associated with a reduced risk of developing progressive multifocal leukoencephalopathy during treatment with natalizumab. Ann Neurol. 2015;77:447-57.
13. Fissolo N, Pignolet B, Matute-Blanch C, Trivino JC, Miro B, Mota M. Matrix Metalloproteinase 9 Is Decreased in Natalizumab-Treated Multiple Sclerosis Patients at Risk for Progressive Multifocal Leukoencephalopathy. Ann Neurol. 2017;82:186-95.
14. Bielekova B, Becker BL. Monoclonal antibodies in MS: mechanisms of action. Neurology. 2010;74(Suppl 1):S31-S40.
15. Hu Y, Turner MJ, Shields J, Gale MS, Hutto E, Roberts BL, et al. Investigation of the mechanism of action of alemtuzumab in a human CD52 transgenic mouse model. Immunology. 2009;128:260-70. 16. Ziemssen T, Thomas K. Alemtuzumab in the long-term treatment of relapsing-remitting multiple sclerosis: an update on the clinical trial evidence and data from the real world. Ther Adv Neurol
Disord. 2017;10:343-59.
17. Jones JL, Anderson JM, Phuah CL, Fox EJ, Selmaj K, Margolin D, et al. Improvement indisability
after alemtuzumab treatment of multiple sclerosis is associated with neuroprotective autoimmunity.
Brain. 2010;133(Pt 8):2232-47.
18. Jones JL, Phuah CL, Cox AL, Thompson SA, Ban M, Shawcross J, et al. IL-21 drives secondary
autoimmunity in patients with multiple sclerosis, following therapeutic lymphocyte depletion with alemtuzumab(Campath-1H). J Clin Invest. 2009;119:2052-61.
81