Monocytes and CD4+ T cells contribution to the under-expression of NR4A2 and TNFAIP3 genes in patients with multiple sclerosis.
We recently found a gene signature for multiple sclerosis (MS) that reverted to normal during pregnancy in MS patients and included NR4A2 and TNFAIP3, key molecules in anti-inflammatory processes. Here we focus on the expression levels of these two genes in monocytes and CD4+ T cells from healthy controls and treatment-naïve RRMS patients. Our findings show that monocytes play a key role in the dysregulated anti-inflammatory response, being the expression of both genes down-regulated in these cells in RRMS patients with respect to healthy individuals. CD4+ T cells seem to have only a marginal part, because we can observe only a slight down-regulation in NR4A2.
Neurology Unit 2 - CRESM (Regional Referring Center of Multiple Sclerosis), Neuroscience Institute Cavalieri Ottolenghi (NICO) University of Turin, AOU San Luigi Gonzaga, 10043 Orbassano, Turin, Italy. Electronic address: nicolednavone@gmail.com.
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Navone
Neurology Unit 2 - CRESM (Regional Referring Center of Multiple Sclerosis), Neuroscience Institute Cavalieri Ottolenghi (NICO) University of Turin, AOU San Luigi Gonzaga, 10043 Orbassano, Turin, Italy.
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Perga
Neurology Unit 2 - CRESM (Regional Referring Center of Multiple Sclerosis), Neuroscience Institute Cavalieri Ottolenghi (NICO) University of Turin, AOU San Luigi Gonzaga, 10043 Orbassano, Turin, Italy.
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Martire
Department of Clinical and Biological Sciences, University of Turin, Torino, Italy.
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Berchialla
Neurology Unit 2 - CRESM (Regional Referring Center of Multiple Sclerosis), Neuroscience Institute Cavalieri Ottolenghi (NICO) University of Turin, AOU San Luigi Gonzaga, 10043 Orbassano, Turin, Italy.
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Malucchi
Neurology Unit 2 - CRESM (Regional Referring Center of Multiple Sclerosis), Neuroscience Institute Cavalieri Ottolenghi (NICO) University of Turin, AOU San Luigi Gonzaga, 10043 Orbassano, Turin, Italy. Electronic address: antonio.bertolotto@gmail.com.
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Bertolotto
D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D004185:Disability Evaluation; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology*; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D009103:Multiple Sclerosis / Q000473:pathology*; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism*; D057126:Nuclear Receptor Subfamily 4, Group A, Member 2 / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D018709:Statistics, Nonparametric; D000072598:Tumor Necrosis Factor alpha-Induced Protein 3; D055815:Young Adult
D004268:DNA-Binding Proteins; D047908:Intracellular Signaling Peptides and Proteins; C539882:NR4A2 protein, human; D009687:Nuclear Proteins; D057126:Nuclear Receptor Subfamily 4, Group A, Member 2; D012333:RNA, Messenger; C076529:TNFAIP3 protein, human; D000072598:Tumor Necrosis Factor alpha-Induced Protein 3
CD4+ T cells; Monocytes; Multiple sclerosis; NR4A2; TNFAIP3