P-glycoprotein function in peripheral T lymphocyte subsets of myasthenia gravis patients: Clinical implications and influence of glucocorticoid administration |
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Institution: | 1. Department of Diagnostic Imaging, Molecular Imaging, Interventional Radiology and Radiotherapy, Tor Vergata General Hospital, Rome, Italy;2. Unit of Radiation Oncology, Azienda Ospedaliero-Universitaria Careggi, Florence, Italy;1. Trakya University Faculty of Medicine, Department of Ophthalmology, 22030 Edirne, Turkey;2. Trakya University Faculty of Medicine, Department of Medical Biology, 22030 Edirne, Turkey |
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Abstract: | Myasthenia gravis (MG) is an autoimmune neuromuscular disorder with a chronic clinical course that requires long-term glucocorticoid (GC) therapy. A drug efflux pump, P-glycoprotein (P-gp), actively transports GC out of target cells, thereby reducing its efficacy. We evaluated the P-gp function of peripheral-blood mononuclear cells in 59 MG patients. P-gp function was estimated from a decrease in fluorescent P-gp substrate Rhodamine 123 and its inhibition by the conformation-sensitive UIC2 monoclonal antibody. P-gp function on CD8+ T cells in 21 MG patients having experienced GC therapy was higher than that in 19 MG patients having no history of GC therapy (p = 0.026). There was a significant correlation between P-gp function in CD3+ (r = 0.55, p = 0.014) or CD4+ (r = 0.48, p = 0.034) T cells and the total dose of prednisolone for treatment. P-gp function on CD4+ T cells in MG patients who showed low responses to prednisolone therapy (n = 8) was higher than that in patients who showed relatively high responses to prednisolone therapy (n = 10) (p = 0.045). These results suggest that higher P-glycoprotein activity on CD3+ or CD4+ cells necessitated treatment with higher steroid doses in order to achieve a clinical response. The measurement of P-gp function on CD4+ T cells is useful in the assessment of clinical response to GC therapy. |
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