Differential expression of CD150 (SLAM) on monocytes and macrophages in chronic inflammatory contexts: abundant in Crohn's disease, but not in multiple sclerosis.
Journal of Clinical Pathology (impact factor: 2.31). 02/2005; 58(1):110-1. DOI:10.1136/jcp.2004.019323 pp.110-1
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ABSTRACT: An array of design strategies have been targeted toward minimizing failure of implanted microelectrodes by minimizing the chronic glial scar around the microelectrode under chronic conditions. Current approaches toward inhibi-ting the initiation of glial scarring range from altering the geometry, roughness, size, shape, and materials of the device. Studies have shown materials which mimic the nanotopography of the natural environment in vivo will con-sequently result in an improved biocompatible response. Nanofabrication of electrode arrays is being pursued in the field of neuronal electrophysiology to increase sampling capabilities. Literature shows a gap in research of nanoto-pography influence in the reduction of astrogliosis. The aim of this study was to determine optimal feature sizes for neural electrode fabrication, which was defined as eliciting a nonreactive astrocytic response. Nanopatterned surfaces were fabricated with nanoimprint lithography on poly (methyl methacrylate) surfaces. The rate of protein adsorption, quantity of protein adsorption, cell alignment, morphology, adhesion, proliferation, viability, and gene expression was compared between nanopatterned surfaces of different dimensions and non-nanopatterned control surfaces. Results of this study revealed that 3600 nanopat-terned surfaces elicited less of a response when compared with the other patterned and non-nanopatterned surfaces. The surface instigated cell alignment along the nanopattern, less protein adsorption, less cell adhesion, proliferation and viability, inhibition of glial fibrillary acidic protein, and mito-gen-activated protein kinase kinase 1 compared with all other substrates tested. V C 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 101A: 1743–1757, 2013.
Article: High expression of CD244 and SAP regulated CD8 T cell responses of patients with HTLV-I associated neurologic disease.[show abstract] [hide abstract]
ABSTRACT: HTLV-I-specific CD8(+) T cells have been characterized with high frequencies in peripheral blood and cerebrospinal fluid and production of proinflammatory cytokines, which contribute to central nervous system inflammation in HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). However, little is known about the differences in CD8(+) T cell activation status between asymptomatic carrier (ACs) and patients with HAM/TSP. The expression of CD244, a signaling lymphocyte activation molecule (SLAM) family receptor, was significantly higher on CD8(+) T cells in HTLV-I-infected patients, both ACs and patients with HAM/TSP, than those on healthy normal donors (NDs). Blockade of CD244 inhibited degranulation and IFN-gamma production in CD8(+) T cells of patients with HAM/TSP, suggesting that CD244 is associated with effector functions of CD8(+) T cells in patients with HAM/TSP. Moreover, SLAM-associated protein (SAP) was overexpressed in patients with HAM/TSP compared to ACs and NDs. SAP expression in Tax-specific CTLs was correlated in the HTLV-I proviral DNA loads and the frequency of the cells in HTLV-I-infected patients. SAP knockdown by siRNA also inhibited IFN-gamma production in CD8(+) T cells of patients with HAM/TSP. Thus, the CD244/SAP pathway was involved in the active regulation of CD8(+) T cells of patients with HAM/TSP, and may play roles in promoting inflammatory neurological disease.PLoS Pathogens 12/2009; 5(12):e1000682. · 9.13 Impact Factor
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