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01000naa a22002652 4500 |
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NLM163421803 |
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DE-627 |
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20231223100316.0 |
| 007 |
tu |
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231223s2006 xx ||||| 00| ||eng c |
| 028 |
5 |
2 |
|a pubmed24n0545.xml
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|a (DE-627)NLM163421803
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| 035 |
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|a (NLM)16765091
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Rozkova, Daniela
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a Glucocorticoids severely impair differentiation and antigen presenting function of dendritic cells despite upregulation of Toll-like receptors
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| 264 |
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1 |
|c 2006
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| 336 |
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|a Text
|b txt
|2 rdacontent
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| 337 |
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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| 338 |
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|a Band
|b nc
|2 rdacarrier
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| 500 |
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|a Date Completed 26.09.2006
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| 500 |
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|a Date Revised 09.04.2022
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| 500 |
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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| 520 |
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|a Glucocorticoids (GCs) are widely used as anti-inflammatory and immunosuppressive agents. Effects of GC have mainly been attributed to the suppression of T cells. Recently, several studies have indicated the role of dendritic cells (DC) in GC-mediated immunosuppression. We investigated the effect of GC on characteristics of DC. Given the crucial role of Toll-like receptor (TLR) triggering for the initiation of DC maturation program, we analyzed the expression of TLR2, 3, 4 by GC-treated DC. To extend our in vitro findings, we analyzed the distribution of DC subsets in the blood of patients treated with high-dose corticosteroids. DC differentiation in presence of GC was skewed to a qualitatively distinct population incapable of inducing an efficient immune response, whereas GC presence during the process of maturation significantly reduced DC IL-12 p70 and TNF production and T cell stimulatory function. Despite the fact that GC increased expression of TLR2, 3 and 4 on DC, their stimulation with TLR-derived signals did not induce maturation. Administration of high-dose GC to the patients with systemic autoimmunity induced a decrease of circulating myeloid DC and abrogated plasmacytoid DC. These findings provide further insights into the mechanisms of GC immunosuppressive functions and reveal additional mechanisms of their therapeutic efficiency
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| 650 |
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4 |
|a Journal Article
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| 650 |
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4 |
|a Research Support, Non-U.S. Gov't
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| 650 |
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7 |
|a Cytokines
|2 NLM
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| 650 |
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7 |
|a Glucocorticoids
|2 NLM
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| 650 |
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7 |
|a Toll-Like Receptors
|2 NLM
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| 650 |
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7 |
|a Dexamethasone
|2 NLM
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| 650 |
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7 |
|a 7S5I7G3JQL
|2 NLM
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| 650 |
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7 |
|a Prednisone
|2 NLM
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| 650 |
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7 |
|a VB0R961HZT
|2 NLM
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| 650 |
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7 |
|a Methylprednisolone
|2 NLM
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| 650 |
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7 |
|a X4W7ZR7023
|2 NLM
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| 700 |
1 |
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|a Horvath, Rudolf
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Bartunkova, Jirina
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Spisek, Radek
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 120(2006), 3 vom: 15. Sept., Seite 260-71
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:120
|g year:2006
|g number:3
|g day:15
|g month:09
|g pages:260-71
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| 912 |
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|a GBV_USEFLAG_A
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| 912 |
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|a SYSFLAG_A
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| 912 |
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|a GBV_NLM
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| 912 |
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|a GBV_ILN_24
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| 912 |
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|a GBV_ILN_350
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| 951 |
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|a AR
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| 952 |
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|d 120
|j 2006
|e 3
|b 15
|c 09
|h 260-71
|