Selective resistance to different glucocorticoids in severe autoimmune disorders
2009 Elsevier Inc. All rights reserved.
Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 134(2010), 3 vom: 18. März, Seite 313-9 |
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1. Verfasser: | |
Weitere Verfasser: | , , , , , |
Format: | Online-Aufsatz |
Sprache: | English |
Veröffentlicht: |
2010
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Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
Schlagworte: | Journal Article Research Support, Non-U.S. Gov't ATP Binding Cassette Transporter, Subfamily B, Member 1 Formazans Glucocorticoids Multidrug Resistance-Associated Proteins Tetrazolium Salts MTT formazan 23305-68-2 DNA mehr... |
Zusammenfassung: | 2009 Elsevier Inc. All rights reserved. Resistance to glucocorticoids often occurs in patients with severe inflammatory disorders. Occasionally, this resistance could be overcome by switching to a different glucocorticoid, but the mechanisms of this selectivity are not clear. We studied this condition in three patients with severe inflammatory disorders, who responded satisfactorily to betamethasone, but could not be switched to equipotent doses of methylprednisolone or prednisone. While betamethasone displayed similar activity on lymphocyte proliferation in cells obtained from the three patients and controls, higher concentrations of methylprednisolone were needed to inhibit proliferation in patients' cells. In a competition study, the concentration of methylprednisolone that inhibited 50% of specific [(3)H]dexamethasone binding was increased in patients' lymphocytes. Higher Rhodamine-123 efflux was demonstrated in CD4 T cells from two patients, suggesting that an increased activity of membrane transporters could be responsible for the selective response to different glucocorticoids, even if P-glycoprotein and MRP1 expression was not increased |
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Beschreibung: | Date Completed 18.03.2010 Date Revised 01.12.2018 published: Print-Electronic Citation Status MEDLINE |
ISSN: | 1521-7035 |
DOI: | 10.1016/j.clim.2009.11.005 |