title: Enhancement of membrane B7-H3 costimulatory molecule but reduction of its soluble form in multiple sclerosis.
abstract: OBJECTIVE
  Multiple sclerosis (MS) is an autoimmune disease of the central nervous system mediated by T cells. B7-H3 plays a diverse role in regulating T cell responses. However, its expression and clinical significance in MS are not well known. This study analyzed the expression of membrane B7-H3 (mB7-H3) and levels of soluble B7-H3 (sB7-H3) in MS patients to determine its clinical significance.
  
  
  METHODS
  Peripheral blood (PB) or cerebrospinal fluid (CSF) samples from healthy controls, other noninflammatory neurological disorders, viral encephalitis, and MS patients were collected. Expression of mB7-H3 on immune cells was detected by flow cytometry. Levels of sB7-H3 in serum or CSF samples were measured by ELISA.
  
  
  RESULTS
  mB7-H3 expression was up-regulated in CSF from MS patients compared to PB (p<0.001). However, serum or CSF levels of sB7-H3 in MS patients were significantly lower than those in controls (p<0.05). Relapsing-MS patients had higher CSF mB7-H3 expression than the remitting subgroup. Relapsing-MS patients had decreased serum and CSF sB7-H3 levels compared with the remitting subgroup. Neurological deficits showed negative correlations with serum or CSF sB7-H3 levels, but a positive correlation with CSF mB7-H3 expression. Methylprednisolone therapy significantly elevated sB7-H3 levels and reduced mB7-H3 expression compared with pre-therapy levels. sB7-H3 levels did not correlate with mB7-H3 expression.
  
  
  CONCLUSIONS
  We demonstrated enhanced mB7-H3 expression and reduced sB7-H3 levels in MS patients which correlated with the clinical characteristics of MS patients. These results suggest that B7-H3 may be a promising biomarker and associated with the pathogenesis of MS.
authors.affiliation: Institute of Medical Biotechnology, Medical College of Soochow University, Suzhou, Jiangsu, 215007, China.
authors.forename: Juean
authors.initials: J
authors.lastname: Jiang
authors.forename: Jianhua
authors.initials: J
authors.lastname: Jiang
authors.forename: Cuiping
authors.initials: C
authors.lastname: Liu
authors.forename: Guangbo
authors.initials: G
authors.lastname: Zhang
authors.forename: Li
authors.initials: L
authors.lastname: Gao
authors.forename: Yongjing
authors.initials: Y
authors.lastname: Chen
authors.forename: Ranran
authors.initials: R
authors.lastname: Zhu
authors.forename: Ting
authors.initials: T
authors.lastname: Wang
authors.forename: Fengmin
authors.initials: F
authors.lastname: Wang
authors.forename: Xueguang
authors.initials: X
authors.lastname: Zhang
authors.forename: Qun
authors.initials: Q
authors.lastname: Xue
mesh_terms: D060887:B7 Antigens / Q000037:antagonists & inhibitors* / Q000096:biosynthesis* / Q000134:cerebrospinal fluid; D015415:Biomarkers / Q000097:blood / Q000134:cerebrospinal fluid; D015536:Down-Regulation / Q000235:genetics / Q000276:immunology*; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D006801:Humans; D008297:Male; D008562:Membrane Glycoproteins / Q000037:antagonists & inhibitors* / Q000096:biosynthesis* / Q000134:cerebrospinal fluid; D009103:Multiple Sclerosis / Q000134:cerebrospinal fluid / Q000209:etiology / Q000276:immunology*; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000134:cerebrospinal fluid / Q000209:etiology / Q000276:immunology; D020033:Protein Isoforms / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000134:cerebrospinal fluid; D012995:Solubility; D015854:Up-Regulation / Q000276:immunology*
chemical_list: D060887:B7 Antigens; D015415:Biomarkers; C423237:CD276 protein, human; D008562:Membrane Glycoproteins; D020033:Protein Isoforms