CD4+/CD45RO+: A Potential Biomarker of the Clinical Response to Glatiramer Acetate
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
31096621
PubMed Central
PMC6562382
DOI
10.3390/cells8050456
PII: cells8050456
Knihovny.cz E-zdroje
- Klíčová slova
- CD4+/CD45RO+, biomarker, disease progression, glatiramer acetate, multiple sclerosis, patients,
- MeSH
- antigeny CD45 krev MeSH
- biologické markery MeSH
- biomarkery farmakologické MeSH
- diferenciační antigeny krev MeSH
- dospělí MeSH
- glatiramer acetát terapeutické užití MeSH
- kohortové studie MeSH
- lidé středního věku MeSH
- lidé MeSH
- lymfocyty imunologie MeSH
- mladý dospělý MeSH
- počet lymfocytů metody MeSH
- progrese nemoci MeSH
- roztroušená skleróza farmakoterapie imunologie MeSH
- senioři MeSH
- výsledek terapie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- antigeny CD45 MeSH
- biologické markery MeSH
- biomarkery farmakologické MeSH
- diferenciační antigeny MeSH
- glatiramer acetát MeSH
Background: Glatiramer acetate (GA) is an effective treatment for the earliest stages of multiple sclerosis (MS)-clinically isolated syndrome (CIS) or clinically definite MS (CDMS). Objective: This study aims to determine the differences in the lymphocyte population (at baseline and the course of five years) between confirmed sustained progression (CSP) and non-CSP groups and to identify potential biomarkers among these parameters that can predict a positive response to the treatment. Methods: Twelve male and 60 female patients were included in the study. Peripheral blood samples were collected before and five years after treatment with GA. The authors compared lymphocyte parameters between the CSP and non-CSP groups by statistical analyses. Univariate and penalized logistic regression models were fitted to identify the best lymphocyte parameters at baseline and their combination for potential biomarkers. Subsequently, the ROC analysis was used to identify cut-offs for selected parameters. Results: The parameter CD4+/CD45RO+ was identified as the best single potential biomarker, demonstrating the ability to identify patients with CSP. Moreover, a combination of four lymphocyte parameters at baseline, relative lymphocyte counts, CD3+/CD69+, CD4+/CD45RO+, and CD4+/CD45RA+ab, was identified as a potential composite biomarker. This combination explains 23% of the variability in CSP, which is better than the best univariate parameter when compared to CD4+/CD45RO+ at baseline. Conclusions: The results suggest that other biomarkers can help monitor the conditions of patients and predict a favourable outcome.
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Boneschi F.M., Rovaris M., Johnson K.P., Miller A., Wolinsky J.S., Ladkani D., Shifroni G., Comi G., Filippi M. Effects of glatiramer acetate on relapse rate and accumulated disability in multiple sclerosis: Meta-analysis of three double-blind, randomized, placebo-controlled clinical trials. Mult. Scler. J. 2003;9:349–355. doi: 10.1191/1352458503ms932oa. PubMed DOI
Comi G., Martinelli V., Rodegher M., Moiola L., Bajenaru O., Carra A., Elovaara I., Fazekas F., Hartung H.P., Hillert J., et al. 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;374:1503–1511. doi: 10.1016/S0140-6736(09)61259-9. PubMed DOI
Khan O., Rieckmann P., Boyko A., Selmaj K., Zivadinov R., GALA Study Group Three times weekly glatiramer acetate in relapsing-remitting multiple sclerosis. Ann. Neurol. 2013;73:705–713. doi: 10.1002/ana.23938. PubMed DOI
Khan O., Rieckmann P., Boyko A., Selmaj K., Ashtamker N., Davis M.D., Kolodny S., Zivadinov R. Efficacy and safety of a three-times-weekly dosing regimen of glatiramer acetate in relapsing-remitting multiple sclerosis patients: 3-year results of the Glatiramer Acetate Low-Frequency Administration open-label extension study. Mult. Scler. 2017;23:818–829. doi: 10.1177/1352458516664033. PubMed DOI
Schrempf W., Ziemssen T. Glatiramer acetate: Mechanisms of action in multiple sclerosis. Autoimmun. Rev. 2007;6:469–475. doi: 10.1016/j.autrev.2007.02.003. PubMed DOI
Veugelers P., Fisk J., Brown M., Stadnyk K., Sketris I., Murray T., Bhan V., Sketris I. Disease progression among multiple sclerosis patients before and during a disease-modifying drug program: A longitudinal population-based evaluation. Mult. Scler. J. 2009;15:1286–1294. doi: 10.1177/1352458509350307. PubMed DOI
Ford C., Goodman A.D., Johnson K., Kachuck N., Lindsey J.W., Lisak R., Luzzio C., Myers L., Panitch H., Preiningerova J., et al. Continuous long-term immunomodulatory therapy in relapsing multiple sclerosis: Results from the 15-year analysis of the US prospective open-label study of glatiramer acetate. Mult. Scler. 2010;16:342–350. doi: 10.1177/1352458509358088. PubMed DOI PMC
Munari L., Lovati R., Boiko A. Therapy with glatiramer acetate for multiple sclerosis. Cochrane Database Syst. Rev. 2004:CD004678. doi: 10.1002/14651858.CD004678. PubMed DOI
Polman C.H., Reingold S.C., Edan G., Filippi M., Hartung H.-P., Kappos L., Lublin F.D., Metz L.M., McFarland H.F., O’Connor P.W., et al. Diagnostic criteria for multiple sclerosis: 2005 revisions to the “McDonald Criteria”. Ann. Neurol. 2005;58:840–846. doi: 10.1002/ana.20703. PubMed DOI
Polman C.H., Reingold S.C., Banwell B., Clanet M., Cohen J.A., Filippi M., Fujihara K., Havrdova E.K., Hutchinson M., Kappos L., et al. Diagnostic criteria for multiple sclerosis: 2010 Revisions to the McDonald criteria. Ann. Neurol. 2011;69:292–302. doi: 10.1002/ana.22366. PubMed DOI PMC
Vališ M., Vyšata O., Sobíšek L., Klímová B., Andrýs C., Vokurková D., Pavelek Z. Monitoring of Lymphocyte Populations During Treatment with Interferon-β-1b to Predict Multiple Sclerosis Disability Progression. J. Interferon Cytokine Res. 2018;39:164–173. doi: 10.1089/jir.2018.0100. PubMed DOI
R Core Team . R: A Language and Environment for Statistical Computing. R Foundation for Statistical Computing; Vienna, Austria: 2017.
Friedman J.H., Hastie T., Tibshirani R. Regularization Paths for Generalized Linear Models via Coordinate Descent. J. Stat. Softw. 2010;33:1–22. doi: 10.18637/jss.v033.i01. PubMed DOI PMC
Barrau M.A., Montalban X., Sáez-Torres I., Brieva L., Barberà N., Martínez-Cáceres E.M. CD4(+)CD45RO(+)CD49d(high) cells are involved in the pathogenesis of relapsing-remitting multiple sclerosis. J. Neuroimmunol. 2000;111:215–223. doi: 10.1016/S0165-5728(00)00357-X. PubMed DOI
Beynon V., Quintana F.J., Weiner H.L. Activated human CD4+CD45RO+ memory T-cells indirectly inhibit NLRP3 inflammasome activation through downregulation of P2X7R signalling. PLoS ONE. 2012;7:e39576. doi: 10.1371/journal.pone.0039576. PubMed DOI PMC
Blanco Y., Moral E., Costa M., Gómez-Choco M., Torres-Peraza J., Alonso-Magdalena L., Alberch J., Jaraquemada D., Arbizu T., Graus F., et al. Effect of glatiramer acetate (Copaxone®) on the immunophenotypic and cytokine profile and BDNF production in multiple sclerosis: A longitudinal study. Neurosci. Lett. 2006;406:270–275. doi: 10.1016/j.neulet.2006.07.043. PubMed DOI
Pavelek Z., Vyšata O., Sobíšek L., Klímová B., Andrýs C., Vokurková D., Mazurová R., Štourač P., Vališ M. Lymphocyte populations and their change during five-year glatiramer acetate treatment. Neurol. Neurochir. Pol. 2018;52:587–592. doi: 10.1016/j.pjnns.2018.08.001. PubMed DOI
Valenzuela R.M., Kaufman M., Balashov K.E., Ito K., Buyske S., Dhib-Jalbut S. Predictive cytokine biomarkers of clinical response to glatiramer acetate therapy in multiple sclerosis. J. Neuroimmunol. 2016;15:59–65. doi: 10.1016/j.jneuroim.2016.06.005. PubMed DOI
Mindur J.E., Valenzuela R.M., Yadav S.K., Boppana S., Dhib-Jalbut S., Ito K. IL-27: A potential biomarker for responders to glatiramer acetate therapy. J. Neuroimmunol. 2017;15:21–28. doi: 10.1016/j.jneuroim.2016.07.004. PubMed DOI
Kruszewski A.M., Rao G., Tatomir A., Hewes D., Tegla C.A., Cudrici C.D., Nguyen V., Royal W., 3rd, Bever C.T., Jr., Rus V., et al. RGC-32 as a potential biomarker of relapse and response to treatment with glatiramer acetate in multiple sclerosis. Exp. Mol. Pathol. 2015;99:498–505. doi: 10.1016/j.yexmp.2015.09.007. PubMed DOI PMC
Tatomir A., Talpos-Caia A., Anselmo F., Kruszewski A.M., Boodhoo D., Rus V., Rus H. The complement system as a biomarker of disease activity and response to treatment in multiple sclerosis. Immunol. Res. 2017;65:1103–1109. doi: 10.1007/s12026-017-8961-8. PubMed DOI PMC
Hewes D., Tatomir A., Kruszewski A.M., Rao G., Tegla C.A., Ciriello J., Nguyen V., Royal W., 3rd, Bever C.T., Jr., Rus V., et al. SIRT1 as a potential biomarker of response to treatment with glatiramer acetate in multiple sclerosis. Exp. Mol. Pathol. 2017;102:191–197. doi: 10.1016/j.yexmp.2017.01.014. PubMed DOI
Ciriello J., Tatomir A., Hewes D., Boodhoo D., Anselmo F., Rus V., Rus H. Phosphorylated SIRT1 as a biomarker of relapse and response to treatment with glatiramer acetate in multiple sclerosis. Exp. Mol. Pathol. 2018;105:175–180. doi: 10.1016/j.yexmp.2018.07.008. PubMed DOI
Tumani H., Kassubek J., Hijazi M., Lehmensiek V., Unrath A., Süssmuth S., Lauda F., Kapfer T., Fang L., Senel M., et al. Patterns of TH1/TH2 cytokines predict clinical response in multiple sclerosis patients treated with glatiramer acetate. Eur. Neurol. 2011;65 doi: 10.1159/000324035. PubMed DOI
Lublin F.D., Reingold S.C., Cohen J.A., Cutter G.R., Sørensen P.S., Thompson A.J., Wolinsky J.S., Balcer L.J., Banwell B., Barkhof F., et al. Defining the clinical course of multiple sclerosis: The 2013 revisions. Neurology. 2014;83:278–286. doi: 10.1212/WNL.0000000000000560. PubMed DOI PMC
Zetterberg H., Teunissen C. Fluid biomarkers for disease activity in multiple sclerosis. Mult. Scler. J. 2017;23:1660–1661. doi: 10.1177/1352458517736151. PubMed DOI