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|a pubmed24n0567.xml
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|a (DE-627)NLM170104494
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|a (NLM)17482516
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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1 |
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|a Takahashi, Hideo Kohka
|e verfasserin
|4 aut
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1 |
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|a Action profiles of statins and calcineurin inhibitors during human mixed lymphocyte reaction
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|c 2007
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|a Text
|b txt
|2 rdacontent
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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|a Band
|b nc
|2 rdacarrier
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|a Date Completed 27.08.2007
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|a Date Revised 01.12.2018
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a The cell-to-cell interaction through binding intercellular adhesion molecule (ICAM)-1 and CD40 on monocytes and their ligands such as lymphocyte function-associated antigen (LFA)-1 and CD40 ligand (CD40L) on T-cells plays roles in cytokine production and T-cell proliferation. Interleukin (IL)-18, which is elevated in the plasma during acute rejection after organ transplantation, induces the expression of ICAM-1 and CD40 on monocytes, the production of interferon (IFN)-gamma and IL-12 and the proliferation of T-cells during the human mixed lymphocyte reaction (MLR). In addition to the cholesterol lowering effect, statins improve patient survival and decrease rejection episodes in transplant recipients. In the present study, we investigated the difference of effect of statins and calcineurin inhibitors during MLR. 3-Hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase inhibitors, fluvastatin and pravastatin and statin-derived LFA-1 inhibitors, LFA703 and LFA878, which did not inhibit HMG-CoA reductase, suppressed the production of IFN-gamma and IL-12 and the lymphocyte proliferation as well as the expression of ICAM-1 and CD40 on monocytes regardless of the presence of IL-18. However, the calcineurin inhibitors, tacrolimus and cyclosporine A (CsA), inhibited the IL-18-enhanced cytokine production and lymphocyte proliferation without any effect on the adhesion molecule expression. Thus, the action mechanism of stain is different from that of calcineurin inhibitors
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|a Journal Article
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|a CD40 Antigens
|2 NLM
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7 |
|a Calcineurin Inhibitors
|2 NLM
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|a Fatty Acids, Monounsaturated
|2 NLM
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7 |
|a Hydroxymethylglutaryl-CoA Reductase Inhibitors
|2 NLM
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650 |
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7 |
|a Immunosuppressive Agents
|2 NLM
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650 |
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7 |
|a Indoles
|2 NLM
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7 |
|a Interleukin-18
|2 NLM
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7 |
|a LFA 878
|2 NLM
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7 |
|a LFA703
|2 NLM
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7 |
|a Naphthalenes
|2 NLM
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7 |
|a Oxazines
|2 NLM
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7 |
|a Intercellular Adhesion Molecule-1
|2 NLM
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650 |
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7 |
|a 126547-89-5
|2 NLM
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7 |
|a Interleukin-12
|2 NLM
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650 |
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7 |
|a 187348-17-0
|2 NLM
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650 |
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7 |
|a Fluvastatin
|2 NLM
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650 |
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7 |
|a 4L066368AS
|2 NLM
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7 |
|a Interferon-gamma
|2 NLM
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7 |
|a 82115-62-6
|2 NLM
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7 |
|a Cyclosporine
|2 NLM
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7 |
|a 83HN0GTJ6D
|2 NLM
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7 |
|a Hydroxymethylglutaryl CoA Reductases
|2 NLM
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650 |
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7 |
|a EC 1.1.1.-
|2 NLM
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650 |
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7 |
|a Pravastatin
|2 NLM
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650 |
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7 |
|a KXO2KT9N0G
|2 NLM
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650 |
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7 |
|a Mevalonic Acid
|2 NLM
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650 |
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7 |
|a S5UOB36OCZ
|2 NLM
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650 |
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7 |
|a Tacrolimus
|2 NLM
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650 |
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7 |
|a WM0HAQ4WNM
|2 NLM
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700 |
1 |
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|a Iwagaki, Hiromi
|e verfasserin
|4 aut
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700 |
1 |
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|a Yagi, Takahito
|e verfasserin
|4 aut
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700 |
1 |
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|a Kanke, Toru
|e verfasserin
|4 aut
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700 |
1 |
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|a Liu, Keyue
|e verfasserin
|4 aut
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700 |
1 |
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|a Yoshino, Tadashi
|e verfasserin
|4 aut
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700 |
1 |
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|a Tanaka, Noriaki
|e verfasserin
|4 aut
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700 |
1 |
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|a Nishibori, Masahiro
|e verfasserin
|4 aut
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773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 123(2007), 3 vom: 31. Juni, Seite 324-32
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
1 |
8 |
|g volume:123
|g year:2007
|g number:3
|g day:31
|g month:06
|g pages:324-32
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_11
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|d 123
|j 2007
|e 3
|b 31
|c 06
|h 324-32
|