Peripheral blood lymphocytes immunophenotyping predicts disease activity in clinically isolated syndrome patients

. 2017 Jul 28 ; 17 (1) : 145. [epub] 20170728

Jazyk angličtina Země Velká Británie, Anglie Médium electronic

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/pmid28754092
Odkazy

PubMed 28754092
PubMed Central PMC5534044
DOI 10.1186/s12883-017-0915-1
PII: 10.1186/s12883-017-0915-1
Knihovny.cz E-zdroje

BACKGROUND: Clinically isolated syndrome (CIS) represents first neurological symptoms suggestive of demyelinating lesion in the central nervous system (CNS). Currently, there are no sufficient immunological or genetic markers predicting relapse and disability progression, nor there is evidence of the efficacy of registered disease modifying treatments (DMTs), such as intramuscular interferon beta1a. The aim of the study is to evaluate immunological predictors of a relapse or disability progression. METHODS: One hundred and eighty one patients with CIS were treated with interferon beta1a and followed over the period of 4 years. Lymphocyte subsets were analyzed by flow cytometry. A Kaplan-Meier estimator of survival probability was used to analyze prognosis. For statistical assessment only individual differences between baseline values and values at the time of relapse or confirmed disability progression were analysed. RESULTS: Higher levels of B lymphocytes predicted relapse-free status. On the other hand, a decrease of the naïve subset of cells (CD45RA+ in CD4+) after 12, 24, and 36 months of follow-up were associated with an increased risk of confirmed disability progression. CONCLUSION: Our data suggest that the quantification of lymphocyte subsets in patients after the first demyelinating event suggestive of MS may be an important biomarker.

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Comi G, Martinelli V, Rodegher M, Moiola L, Bajenaru O, Carra A, Elovaara I, Fazekas F, Hartung H, Hillert J. Effect of glatiramer acetate on conversion to clinically definite multiple sclerosis in patients with clinically isolated syndrome (PreCISe study): a randomised, double-blind, placebo-controlled trial. Lancet. 2009;374(9700):1503–1511. doi: 10.1016/S0140-6736(09)61259-9. PubMed DOI

Polman CH, Reingold SC, Edan G, Filippi M, Hartung HP, Kappos L, Lublin FD, Metz LM, McFarland HF, O'Connor PW. Diagnostic criteria for multiple sclerosis: 2005 revisions to the “McDonald criteria”. Ann Neurol. 2005;58(6):840–846. doi: 10.1002/ana.20703. PubMed DOI

Thouvenot É. Update on clinically isolated syndrome. Presse Med. 2015;44(4):e121–e136. doi: 10.1016/j.lpm.2015.03.002. PubMed DOI

Fisniku L, Brex P, Altmann D, Miszkiel K, Benton C, Lanyon R, Thompson A, Miller D. Disability and T2 MRI lesions: a 20-year follow-up of patients with relapse onset of multiple sclerosis. Brain. 2008;131(3):808–817. doi: 10.1093/brain/awm329. PubMed DOI

Dobson R, Rudick RA, Turner B, Schmierer K, Giovannoni G. Assessing treatment response to interferon-β is there a role for MRI. Neurology. 2014;82(3):248–254. doi: 10.1212/WNL.0000000000000036. PubMed DOI PMC

Uher T, Horakova D, Bergsland N, Tyblova M, Ramasamy DP, Seidl Z, Vaneckova M, Krasensky J, Havrdova E, Zivadinov R. MRI correlates of disability progression in patients with CIS over 48 months. NeuroImage: Clinical. 2014;6:312–319. doi: 10.1016/j.nicl.2014.09.015. PubMed DOI PMC

Tumani H, Hartung H-P, Hemmer B, Teunissen C, Deisenhammer F, Giovannoni G, Zettl UK, Group BS Cerebrospinal fluid biomarkers in multiple sclerosis. Neurobiol Dis. 2009;35(2):117–127. doi: 10.1016/j.nbd.2009.04.010. PubMed DOI

Brettschneider J, Tumani H, Kiechle U, Muche R, Richards G, Lehmensiek V, Ludolph AC, Otto M. IgG antibodies against measles, rubella, and varicella zoster virus predict conversion to multiple sclerosis in clinically isolated syndrome. PLoS One. 2009;4(11) doi: 10.1371/journal.pone.0007638. PubMed DOI PMC

Bennett JL, Haubold K, Ritchie AM, Edwards SJ, Burgoon M, Shearer AJ, Gilden DH, Owens GP. CSF IgG heavy-chain bias in patients at the time of a clinically isolated syndrome. J Neuroimmunol. 2008;199(1):126–132. doi: 10.1016/j.jneuroim.2008.04.031. PubMed DOI PMC

Brettschneider J, Czerwoniak A, Senel M, Fang L, Kassubek J, Pinkhardt E, Lauda F, Kapfer T, Jesse S, Lehmensiek V. The chemokine CXCL13 is a prognostic marker in clinically isolated syndrome (CIS) PLoS One. 2010;5(8) doi: 10.1371/journal.pone.0011986. PubMed DOI PMC

Brettschneider J, Petzold A, Süssmuth S, Ludolph A, Tumani H. Axonal damage markers in cerebrospinal fluid are increased in ALS. Neurology. 2006;66(6):852–856. doi: 10.1212/01.wnl.0000203120.85850.54. PubMed DOI

Comabella M, Fernández M, Martin R, Rivera-Vallvé S, Borrás E, Chiva C, Julià E, Rovira A, Cantó E, Alvarez-Cermeño JC. Cerebrospinal fluid chitinase 3-like 1 levels are associated with conversion to multiple sclerosis. Brain. 2010;133(4):1082–1093. doi: 10.1093/brain/awq035. PubMed DOI

Tintore M, Rovira À, Río J, Otero-Romero S, Arrambide G, Tur C, Comabella M, Nos C, Arévalo MJ, Negrotto L: Defining high, medium and low impact prognostic factors for developing multiple sclerosis. Brain 2015:awv105. PubMed

Lassmann H, Ransohoff RM. The CD4–Th1 model for multiple sclerosis: a crucial re-appraisal. Trends Immunol. 2004;25(3):132–137. doi: 10.1016/j.it.2004.01.007. PubMed DOI

Sospedra M, Martin R. Immunology of multiple sclerosis. Annu Rev Immunol. 2005;23:683–747. doi: 10.1146/annurev.immunol.23.021704.115707. PubMed DOI

Rinaldi L, Gallo P, Calabrese M, Ranzato F, Luise D, Colavito D, Motta M, Guglielmo A, Del Giudice E, Romualdi C. Longitudinal analysis of immune cell phenotypes in early stage multiple sclerosis: distinctive patterns characterize MRI-active patients. Brain. 2006;129(8):1993–2007. doi: 10.1093/brain/awl179. PubMed DOI

Kebir H, Ifergan I, Alvarez JI, Bernard M, Poirier J, Arbour N, Duquette P, Prat A. Preferential recruitment of interferon-γ–expressing TH17 cells in multiple sclerosis. Ann Neurol. 2009;66(3):390–402. doi: 10.1002/ana.21748. PubMed DOI

Durelli L, Conti L, Clerico M, Boselli D, Contessa G, Ripellino P, Ferrero B, Eid P, Novelli F. T-helper 17 cells expand in multiple sclerosis and are inhibited by interferon-β. Ann Neurol. 2009;65(5):499–509. doi: 10.1002/ana.21652. PubMed DOI

Zastepa E, Fitz-Gerald L, Hallett M, Antel J, Bar-Or A, Baranzini S, Lapierre Y, Haegert DG. Naive CD4 T-cell activation identifies MS patients having rapid transition to progressive MS. Neurology. 2014;82(8):681–690. doi: 10.1212/WNL.0000000000000146. PubMed DOI PMC

Villar LM, Espiño M, Roldán E, Marín N, Costa-Frossard L, Muriel A, Álvarez-Cermeño JC. Increased peripheral blood CD5+ B cells predict earlier conversion to MS in high-risk clinically isolated syndromes. Mult Scler J. 2011;17(6):690–694. doi: 10.1177/1352458510396922. PubMed DOI

Polman CH, Reingold SC, Banwell B, Clanet M, Cohen JA, Filippi M, Fujihara K, Havrdova E, Hutchinson M, Kappos L. Diagnostic criteria for multiple sclerosis: 2010 revisions to the McDonald criteria. Ann Neurol. 2011;69(2):292–302. doi: 10.1002/ana.22366. PubMed DOI PMC

Kappos L, De Stefano N, Freedman MS, Cree BA, Radue E-W, Sprenger T, Sormani MP, Smith T, Häring DA, Meier DP. Inclusion of brain volume loss in a revised measure of ‘no evidence of disease activity’(NEDA-4) in relapsing–remitting multiple sclerosis. Mult Scler J. 2015;1352458515616701 PubMed PMC

Bongioanni P, Fioretti C, Vanacore R, Bianchi F, Lombardo F, Ambrogi F, Meucci G. Lymphocyte subsets in multiple sclerosis a study with two-colour fluorescence analysis. J Neurol Sci. 1996;139(1):71–77. doi: 10.1016/0022-510X(96)00030-5. PubMed DOI

Mosmann TR, Cherwinski H, Bond MW, Giedlin MA, Coffman RL. Two types of murine helper T cell clone. I. Definition according to profiles of lymphokine activities and secreted proteins. J Immunol. 1986;136(7):2348–2357. PubMed

Constantinescu CS, Gran B. The essential role of T cells in multiple sclerosis: a reappraisal. Biom J. 2014;37(2):34. PubMed

Raphael I, Nalawade S, Eagar TN, Forsthuber TG. T cell subsets and their signature cytokines in autoimmune and inflammatory diseases. Cytokine. 2015;74(1):5–17. PubMed PMC

Eoli M, Ferrarini M, Dufour A, Heltaj S, Bevilacqua L, Comi G, Cosi V, Filippini G, Martinelli V, Milanese C. Presence of T-cell subset abnormalities in newly diagnosed cases of multiple sclerosis and relationship with short-term clinical activity. J Neurol. 1993;240(2):79–82. doi: 10.1007/BF00858721. PubMed DOI

Calopa M, Bas J, Mestre M, Arbizu T, Peres J, Buendia E. T cell subsets in multiple sclerosis: a serial study. Acta Neurol Scand. 1995;92(5):361–368. doi: 10.1111/j.1600-0404.1995.tb00147.x. PubMed DOI

Lehmann D, Karussis D, Mizrachi-Koll R, Linde AS, Abramsky O. Inhibition of the progression of multiple sclerosis by linomide is associated with upregulation of CD4+/CD45RA+ cells and downregulation of CD4+/CD45RO+ cells. Clin Immunol Immunopathol. 1997;85(2):202–209. doi: 10.1006/clin.1997.4444. PubMed DOI

Kreuzfelder E, Shen G, Bittorf M, Scheiermann N, Thraenhart O, Seidel D, Grosse-Wilde H. Enumeration of T, B and natural killer peripheral blood cells of patients with multiple sclerosis and controls. Eur Neurol. 1992;32(4):190–194. doi: 10.1159/000116820. PubMed DOI

Lee-Chang C, Zéphir H, Top I, Dubucquoi S, Trauet J, Prin L, Vermersch P. B-cell subsets up-regulate α4 integrin and accumulate in the cerebrospinal fluid in clinically isolated syndrome suggestive of multiple sclerosis onset. Neurosci Lett. 2011;487(3):273–277. doi: 10.1016/j.neulet.2010.10.036. PubMed DOI

Haas J, Bekeredjian-Ding I, Milkova M, Balint B, Schwarz A, Korporal M, Jarius S, Fritz B, Lorenz H-M, Wildemann B. B cells undergo unique compartmentalized redistribution in multiple sclerosis. J Autoimmun. 2011;37(4):289–299. doi: 10.1016/j.jaut.2011.08.003. PubMed DOI

Disanto G, Morahan J, Barnett M, Giovannoni G, Ramagopalan S. The evidence for a role of B cells in multiple sclerosis. Neurology. 2012;78(11):823–832. doi: 10.1212/WNL.0b013e318249f6f0. PubMed DOI PMC

Ramgolam VS, Sha Y, Marcus KL, Choudhary N, Troiani L, Chopra M, Markovic-Plese S. B cells as a therapeutic target for IFN-β in relapsing–remitting multiple sclerosis. J Immunol. 2011;186(7):4518–4526. doi: 10.4049/jimmunol.1000271. PubMed DOI

Seidi O, Semra Y, Sharief M. Expression of CD5 on B lymphocytes correlates with disease activity in patients with multiple sclerosis. J Neuroimmunol. 2002;133(1):205–210. doi: 10.1016/S0165-5728(02)00360-0. PubMed DOI

Niino M, Hirotani M, Miyazaki Y, Sasaki H. Memory and naive B-cell subsets in patients with multiple sclerosis. Neurosci Lett. 2009;464(1):74–78. doi: 10.1016/j.neulet.2009.08.010. PubMed DOI

De Jager PL, Rossin E, Pyne S, Tamayo P, Ottoboni L, Viglietta V, Weiner M, Soler D, Izmailova E, Faron-Yowe L. Cytometric profiling in multiple sclerosis uncovers patient population structure and a reduction of CD8low cells. Brain. 2008;131(7):1701–1711. doi: 10.1093/brain/awn118. PubMed DOI PMC

Martinez-Rodriguez J, Lopez-Botet M, Munteis E, Rio J, Roquer J, Montalban X, Comabella M. Natural killer cell phenotype and clinical response to interferon-beta therapy in multiple sclerosis. Clin Immunol. 2011;141(3):348–356. doi: 10.1016/j.clim.2011.09.006. PubMed DOI

Hamann I, Dörr J, Glumm R, Chanvillard C, Janssen A, Millward JM, Paul F, Ransohoff RM, Infante-Duarte C. Characterization of natural killer cells in paired CSF and blood samples during neuroinflammation. J Neuroimmunol. 2013;254(1):165–169. doi: 10.1016/j.jneuroim.2012.08.009. PubMed DOI

Bielekova B, Catalfamo M, Reichert-Scrivner S, Packer A, Cerna M, Waldmann TA, McFarland H, Henkart PA, Martin R. Regulatory CD56bright natural killer cells mediate immunomodulatory effects of IL-2Rα-targeted therapy (daclizumab) in multiple sclerosis. Proc Natl Acad Sci. 2006;103(15):5941–5946. doi: 10.1073/pnas.0601335103. PubMed DOI PMC

Saraste M, Irjala H, Airas L. Expansion of CD56Bright natural killer cells in the peripheral blood of multiple sclerosis patients treated with interferon-beta. Neurol Sci. 2007;28(3):121–126. doi: 10.1007/s10072-007-0803-3. PubMed DOI

Vandenbark AA, Huan J, Agotsch M, La Tocha D, Goelz S, Offner H, Lanker S, Bourdette D. Interferon-beta-1a treatment increases CD56 bright natural killer cells and CD4+ CD25+ Foxp3 expression in subjects with multiple sclerosis. J Neuroimmunol. 2009;215(1):125–128. doi: 10.1016/j.jneuroim.2009.08.007. PubMed DOI

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