The low EOMES/TBX21 molecular phenotype in multiple sclerosis reflects CD56+ cell dysregulation and is affected by immunomodulatory therapies

The low EOMES/TBX21 molecular phenotype in multiple sclerosis reflects CD56+ cell dysregulation and is affected by immunomodulatory therapies

Crown Copyright © 2016. Published by Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 163(2016) vom: 05. Feb., Seite 96-107
1. Verfasser: McKay, Fiona C (VerfasserIn)
Weitere Verfasser: Gatt, Prudence N, Fewings, Nicole, Parnell, Grant P, Schibeci, Stephen D, Basuki, Monica A I, Powell, Joseph E, Goldinger, Anita, Fabis-Pedrini, Marzena J, Kermode, Allan G, Burke, Therese, Vucic, Steve, Stewart, Graeme J, Booth, David R
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2016
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Biomarker EOMES Gene expression MS risk gene Multiple sclerosis Natalizumab TBX21 CD56 Antigen mehr... EOMES protein, human Epstein-Barr Virus Nuclear Antigens HLA-DRB1 Chains HLA-DRB1*15:01 antigen Immunologic Factors Immunosuppressive Agents NCAM1 protein, human T-Box Domain Proteins T-box transcription factor TBX21 Glatiramer Acetate 5M691HL4BO Interferon-beta 77238-31-4 Dimethyl Fumarate FO2303MNI2 Fingolimod Hydrochloride G926EC510T EBV-encoded nuclear antigen 1 O5GA75RST7
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100 1 |a McKay, Fiona C  |e verfasserin  |4 aut 
245 1 4 |a The low EOMES/TBX21 molecular phenotype in multiple sclerosis reflects CD56+ cell dysregulation and is affected by immunomodulatory therapies 
264 1 |c 2016 
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500 |a Date Completed 28.06.2016 
500 |a Date Revised 24.09.2018 
500 |a published: Print-Electronic 
500 |a Citation Status MEDLINE 
520 |a Crown Copyright © 2016. Published by Elsevier Inc. All rights reserved. 
520 |a Multiple Sclerosis (MS) is an autoimmune disease treated by therapies targeting peripheral blood cells. We previously identified that expression of two MS-risk genes, the transcription factors EOMES and TBX21 (ET), was low in blood from MS and stable over time. Here we replicated the low ET expression in a new MS cohort (p<0.0007 for EOMES, p<0.028 for TBX21) and demonstrate longitudinal stability (p<10(-4)) and high heritability (h(2)=0.48 for EOMES) for this molecular phenotype. Genes whose expression correlated with ET, especially those controlling cell migration, further defined the phenotype. CD56+ cells and other subsets expressed lower levels of Eomes or T-bet protein and/or were under-represented in MS. EOMES and TBX21 risk SNP genotypes, and serum EBNA-1 titres were not correlated with ET expression, but HLA-DRB1*1501 genotype was. ET expression was normalised to healthy control levels with natalizumab, and was highly variable for glatiramer acetate, fingolimod, interferon-beta, dimethyl fumarate 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a Biomarker 
650 4 |a EOMES 
650 4 |a Gene expression 
650 4 |a MS risk gene 
650 4 |a Multiple sclerosis 
650 4 |a Natalizumab 
650 4 |a TBX21 
650 7 |a CD56 Antigen  |2 NLM 
650 7 |a EOMES protein, human  |2 NLM 
650 7 |a Epstein-Barr Virus Nuclear Antigens  |2 NLM 
650 7 |a HLA-DRB1 Chains  |2 NLM 
650 7 |a HLA-DRB1*15:01 antigen  |2 NLM 
650 7 |a Immunologic Factors  |2 NLM 
650 7 |a Immunosuppressive Agents  |2 NLM 
650 7 |a NCAM1 protein, human  |2 NLM 
650 7 |a Natalizumab  |2 NLM 
650 7 |a T-Box Domain Proteins  |2 NLM 
650 7 |a T-box transcription factor TBX21  |2 NLM 
650 7 |a Glatiramer Acetate  |2 NLM 
650 7 |a 5M691HL4BO  |2 NLM 
650 7 |a Interferon-beta  |2 NLM 
650 7 |a 77238-31-4  |2 NLM 
650 7 |a Dimethyl Fumarate  |2 NLM 
650 7 |a FO2303MNI2  |2 NLM 
650 7 |a Fingolimod Hydrochloride  |2 NLM 
650 7 |a G926EC510T  |2 NLM 
650 7 |a EBV-encoded nuclear antigen 1  |2 NLM 
650 7 |a O5GA75RST7  |2 NLM 
700 1 |a Gatt, Prudence N  |e verfasserin  |4 aut 
700 1 |a Fewings, Nicole  |e verfasserin  |4 aut 
700 1 |a Parnell, Grant P  |e verfasserin  |4 aut 
700 1 |a Schibeci, Stephen D  |e verfasserin  |4 aut 
700 1 |a Basuki, Monica A I  |e verfasserin  |4 aut 
700 1 |a Powell, Joseph E  |e verfasserin  |4 aut 
700 1 |a Goldinger, Anita  |e verfasserin  |4 aut 
700 1 |a Fabis-Pedrini, Marzena J  |e verfasserin  |4 aut 
700 1 |a Kermode, Allan G  |e verfasserin  |4 aut 
700 1 |a Burke, Therese  |e verfasserin  |4 aut 
700 1 |a Vucic, Steve  |e verfasserin  |4 aut 
700 1 |a Stewart, Graeme J  |e verfasserin  |4 aut 
700 1 |a Booth, David R  |e verfasserin  |4 aut 
773 0 8 |i Enthalten in  |t Clinical immunology (Orlando, Fla.)  |d 1999  |g 163(2016) vom: 05. Feb., Seite 96-107  |w (DE-627)NLM098196855  |x 1521-7035  |7 nnns 
773 1 8 |g volume:163  |g year:2016  |g day:05  |g month:02  |g pages:96-107 
856 4 0 |u http://dx.doi.org/10.1016/j.clim.2015.12.015  |3 Volltext 
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