الفهرس 
Studying the possible role of some long noncoding RNAs in multiple sclerosis
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Abstract
Multiple sclerosis (MS) is the primary cause of non-traumatic neurological
disability in young adults. Relapsing-remitting MS (RRMS) is the most prevalent
MS subtype. Ample evidence indicated that long noncoding RNAs (lncRNAs) are
crucial players in autoimmune and inflammatory disorders. Despite the rapidly
increasing data concerning MS-related lncRNAs, the impact of others remains to be
explored. This study investigated for the first time the expression profiles of
lnc-EGFR, SNHG1, and lincRNA-Cox2 in Egyptian patients with RRMS during
active relapses and in remission. Besides, the expression of FOXP3, a master
transcription factor for T-regulatory cells, and the NLRP3 inflammasome-related
genes were determined. Relations between these parameters and MS activity and
annualized relapse rate (ARR) were evaluated. Expression of the three lncRNAs,
FOXP3, NLRP3, ASC, and caspase-1 along with serum TGF-β1and IL-1β levels
were measured in 70 RRMS patients (35 during relapse and 35 in remission) and 30
healthy controls. RRMS patients showed significant downregulation of lnc-EGFR
and FOXP3 together with dramatic upregulation of SNHG1, lincRNA-Cox2,
NLRP3, ASC and caspase-1 expression compared to controls. Lower serum
TGF-β1 and elevated IL-1β levels were observed in RRMS patients. Notably,
patients during relapses displayed more significant alterations than those in
remission. Lnc-EGFR was positively correlated with FOXP3 and TGF-β1, and
negatively correlated with ARR, SNHG1, lincRNA-Cox2 and NLRP3
inflammasome-components. Meanwhile, SNHG1 and lincRNA-Cox2 were
positively correlated with ARR, NLRP3, ASC, caspase-1 and IL-1β. Excellent
diagnostic performance for lnc-EGFR, FOXP3 and TGF-β1 was demonstrated,
while all the biomarkers exhibited strong prognostic potential for predicting
relapses. Finally, the differential expression of lnc-EGFR, SNHG1, and lincRNA-Cox2 in RRMS patients especially during relapses suggests their
involvement in RRMS pathogenesis and activity. Moreover, correlation between
their expression and ARR implies relation to disease progression. Our findings also
highlight their promising roles as biomarkers for RRMS.