The activity of the Golgi glycosyltransferase beta1,6 N-acetylglucosaminyltransferase (core 2 GlcNAc-T), which plays a role in T-cell activation and cell-cell adhesion, appears to be modulated in resting lymphomonocytes during different phases of multiple sclerosis (MS). In particular, a significant decrease (25-30%) of the enzyme activity was observed, with respect to healthy subjects, in MS patients who were in relapse or in the very early stages of remission. A similar trend was found to be associated with patients affected by active lesions. A statistically significant decrease in the enzyme activity was also observed in patients with the progressive form. By contrast, core 2 GlcNAc-T activity did not appear correlated with duration of the disease. Interestingly, MS individuals under treatment with IFN-beta1a, an immunosuppressive agent, showed levels of activity which were comparable with those observed in healthy subjects. Together, these observations suggest that down-regulation of core 2 GlcNAc-T activity is linked to the occurrence of acute phases in the relapsing-remitting form and to the progressive form of the disease, probably caused by altered expression of glycoproteins which are involved in lymphomonocyte activation and/or interaction with the endothelium. Additionally, it appears that the enzyme assay may provide a useful marker of the disease activity and the effects of therapeutical approaches.

Orlacchio, A., Sarchielli, P., Gallai, V., Datti, A., Saccardi, C., Palmerini, C. (1997). Activity levels of a beta1,6 N-acetylglucosaminyltransferase in lymphomonocytes from multiple sclerosis patients. JOURNAL OF THE NEUROLOGICAL SCIENCES, 151(2), 177-183 [10.1016/S0022-510X(97)00117-2].

Activity levels of a beta1,6 N-acetylglucosaminyltransferase in lymphomonocytes from multiple sclerosis patients

ORLACCHIO, ANTONIO;
1997-10-22

Abstract

The activity of the Golgi glycosyltransferase beta1,6 N-acetylglucosaminyltransferase (core 2 GlcNAc-T), which plays a role in T-cell activation and cell-cell adhesion, appears to be modulated in resting lymphomonocytes during different phases of multiple sclerosis (MS). In particular, a significant decrease (25-30%) of the enzyme activity was observed, with respect to healthy subjects, in MS patients who were in relapse or in the very early stages of remission. A similar trend was found to be associated with patients affected by active lesions. A statistically significant decrease in the enzyme activity was also observed in patients with the progressive form. By contrast, core 2 GlcNAc-T activity did not appear correlated with duration of the disease. Interestingly, MS individuals under treatment with IFN-beta1a, an immunosuppressive agent, showed levels of activity which were comparable with those observed in healthy subjects. Together, these observations suggest that down-regulation of core 2 GlcNAc-T activity is linked to the occurrence of acute phases in the relapsing-remitting form and to the progressive form of the disease, probably caused by altered expression of glycoproteins which are involved in lymphomonocyte activation and/or interaction with the endothelium. Additionally, it appears that the enzyme assay may provide a useful marker of the disease activity and the effects of therapeutical approaches.
22-ott-1997
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore MED/26 - NEUROLOGIA
English
Con Impact Factor ISI
Magnetic Resonance Imaging; Multiple Sclerosis; Humans; Adult; Disease Progression; Golgi Apparatus; N-Acetylglucosaminyltransferases; Lymphocytes; Biological Markers
Orlacchio, A., Sarchielli, P., Gallai, V., Datti, A., Saccardi, C., Palmerini, C. (1997). Activity levels of a beta1,6 N-acetylglucosaminyltransferase in lymphomonocytes from multiple sclerosis patients. JOURNAL OF THE NEUROLOGICAL SCIENCES, 151(2), 177-183 [10.1016/S0022-510X(97)00117-2].
Orlacchio, A; Sarchielli, P; Gallai, V; Datti, A; Saccardi, C; Palmerini, C
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/90023
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