Association between CD24 Ala/Val polymorphism and multiple sclerosis risk

Abstract

Background: The aim of this study was to explore the association between CD24 Ala/Val polymorphism and susceptibility of multiple sclerosis (MS). Methods: A comprehensive literature search for relevant studies was performed on google scholar, PubMed, Web of science, Embase, the Chinese National Knowledge Infrastructure and the Chinese Biology Medicine. This meta-analysis was conducted using the STATA 11.0 software and the pooled odds ratio with 95% confidence interval was calculated. Results: Seven case-control studies were included in this meta-analysis. The results showed significant association between CD24 Ala/Val polymorphism and susceptibility to MS. Stratified analysis by areas also showed significant association in Asians. However, no association was found in Europeans. Conclusion: This study suggested that the CD24 Val allele was associated with an increased risk of MS and larger-scale studies of populations are needed to explore the role of CD24 Ala/Val polymorphism during the pathogenesis of MS.

Identification of candidate biomarkers and pathways associated with multiple sclerosis using bioinformatics and next generation sequencing data analysis

“…GO and REACTOME pathway enrichment analyses were used to explore the molecular mechanisms of the genes involved in the occurrence and development of MS. It is well known that the pathways include immune system [55], TCR signaling [56], cytokine signaling in immune system [57], degradation of the extracellular matrix [58], extracellular matrix organization [58], metabolism of lipids [59] and metabolism [60] plays an important role only in MS. CCL18 [61], FCRL3 [62], EOMES (eomesodermin) [63], CCR2 [64], IL2RB [65], CCL4 [66], FASLG (Fas ligand) [67], CD24 [68], IKZF3 [69], CD2 [70], CD28 [71], IL7R [72], HLA-DRB5 [73], ICOS (inducible T cell costimulator) [74], CCL5 [75], CTLA4 [76], IRF4 [77], C6 [78], NCR1 [79], CHIT1 [80], CD52 [81], CD163 [82], HGF (hepatocyte growth factor) [83], DIO3 [84], SIGLEC1 [85], TTR (transthyretin) [86], IL9 [87], VEGFA (vascular endothelial growth factor A) [88], CR2 [89], ANGPTL4 [90], CHI3L1 [91], MAG (myelin associated glycoprotein) [92], CNP (2’,3’-cyclic nucleotide 3’ phosphodiesterase) [93], CMTM5 [94], SEMA4D [95], NGFR (nerve growth factor receptor) [96], TF (transferrin) [97], MYRF (myelin regulatory factor) [98], MOG (myelin oligodendrocyte glycoprotein) [99], ADAMTS4 [100], BMP2 [101], HTRA1 [102], PNPLA3 [103], DYSF (dysferlin) [104], NINJ2 [105], LRP2 [106], ADAMTS14 [107] and DHCR7 [108] might play an important role in regulating the occurrence and development of MS. The expression of CCL18 [109], SLAMF7 [110], GPR174 [111], CCR4 [112], POU4F2 [113].…”

The biological roles of CD24 in ovarian cancer: old story, but new tales

“…CD24 is expressed on a broad range of cells in the central nervous systems (CNS) and is related to the development of experimental autoimmune encephalomyelitis in mice. There are increasing studies focus on the association of a CD24 Ala/Val coding polymorphism with the susceptibility and progression of multiple sclerosis (12). It is reported that CD24 deficient mice could be more susceptible to danger associated molecular patterns but not pathogen-associated molecular patterns.…”