As a proinflammatory cytokine, CD137 (4‐1BB, TNFRSF9) is present in membrane‐bound and soluble forms. Increased expression of CD137 was recently found in T cells in human atherosclerotic plaques. However, the exact role of CD137 in ischemic stroke is not clear. In this study we analyzed the protein levels of soluble CD137 (sCD137) and the expression of CD137 on CD4+ T cells in the peripheral blood of patients with acute atherothrombotic stroke by using the cytometry beads array (CBA) and flow cytometry. Within 24 hours of onset, the stroke patients showed elevated levels of sCD137 (2.7 pg/ml) and CD137 expression on CD4+ T cells (4.9 ± 3.2%) compared with normal controls (1.1 pg/ml, P < 0.01; 1.3 ± 1.0%, P < 0.01). Alterations in CD137 expression may enhance ischemia‐induced inflammatory responses via bidirectional signaling and, consequently, aggravate brain injury in early stages of this disorder.
Multiple sclerosis (MS) and neuromyelitis optica (NMO) are inflammatory demyelinating disorders of the central nervous system (CNS). Various genetic and environmental factors have been identified to contribute to etiology of MS and NMO. Aquaporin 4 (AQP4), is the most abundant water channel in CNS. AQP4 is expressed in astrocytes of the brain, spinal cord, optic nerve and supportive cells in sensory organs. In contrast to MS, immunoreactivity of AQP4 is abolished in NMO lesions. However, conflicting results have been reported regarding the association between AQP4 polymorphisms and demyelinating disorders. Considering the ethnic differences of genetic variations, replications in other cohorts are required. In this study, single nucleotide polymorphisms (SNPs) of AQP4 gene in patients with NMO/neuromyelitis optica spectrum disorders (NMOSD), and MS in the Northern Han Chinese population were examined. Six selected AQP4 SNPs were genotyped by high-resolution melting (HRM) method. Compared with healthy control (HC), there was no significant difference of AQP4 allele and genotype frequency in MS or NMO/NMOSD group. This study showed no significant association of common AQP4 SNPs with MS or NMO/NMOSD, strongly suggesting that polymorphisms of AQP4 gene are unlikely to confer MS or NMO/NMOSD susceptibility, at least in Northern Han Chinese population.
Background: As a member of the tumor necrosis factor superfamily (TNFSF), LIGHT (TNFSF14) is expressed by a variety of immune cells and exists in membrane-bound and soluble forms. Recently, LIGHT was found to be associated with platelets and released upon activation. Activation of endothelia cells by recombinant LIGHT protein results in pro-inflammatory and pro-thrombotic changes. Several studies have reported increased plasma levels of LIGHT in patients with stroke and cardiovascular diseases. However, the form-associated roles of LIGHT in ischemic atherosclerotic stroke remain unclear. Materıals and Methods: In this study, the platelet LIGHT expression and soluble LIGHT protein were analyzed by flow cytometry and enzyme-linked immunosorbent assay (ELISA) in peripheral blood of patients with acute ischemic atherosclerotic stroke, asymptomatic carotid stenosis (ACS) and normal controls. RESULTS: During the initial 24 h after onset, the stroke patients had decreased LIGHT expression on their platelets (5.9% ± 4.9%) and increased plasma LIGHT levels (36.1 ± 21.0 pg/ml) as compared with normal controls (9.5% ± 3.0%, p < 0.05; 20.4 ± 13.4 pg/ml, p < 0.05). Moreover, the platelet LIGHT expression correlated with total plaque area in the stroke patients (r = 0.4572, p = 0.0247). Conclusıons: The dysregulated LIGHT expression reflects a persistent chronic inflammatory response that may have been induced during early stages of ischemic atherosclerotic stroke. Our results strongly suggest distinctive roles of form-associated LIGHT in the disease pathogenesis: platelet-associated LIGHT may contribute to formation and development of carotid atherosclerotic plaque, probably involving
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