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231224s2011 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2011.02.007
|2 doi
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|a pubmed25n0689.xml
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|a (DE-627)NLM206735642
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|a (NLM)21414849
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Kuschei, Werner M
|e verfasserin
|4 aut
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|a Costimulatory signals potently modulate the T cell inhibitory capacity of the therapeutic CD11a antibody Efalizumab
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|c 2011
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 23.06.2011
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|a Date Revised 10.12.2019
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2011 Elsevier Inc. All rights reserved.
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|a The therapeutic CD11a antibody Efalizumab interferes with psoriasis pathogenesis by blocking T cell activation and migration. We have performed a detailed analysis on its effects during the activation of human T cells and found that the capability of Efalizumab to inhibit proliferation and cytokine production of T cells critically depends on the quality and quantity of costimulatory signals. Efalizumab potently inhibited the proliferation and cytokine production of human T cells costimulated via ICOS, OX40, CD27 or 4-1BB, but did not significantly inhibit T cells that received stimuli via CD2 or CD28. The capacity of CD2 and CD28 signals to interfere with the T cell inhibitory effects of Efalizumab was also observed upon stimulation of T cells with allogeneic DC. Furthermore, studies with T cells from psoriasis patients indicated that Efalizumab therapy induces inhibition of T cell responses that can be reverted by CD2 or CD28 signals
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a 4-1BB Ligand
|2 NLM
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|a Antibodies, Monoclonal
|2 NLM
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|a Antibodies, Monoclonal, Humanized
|2 NLM
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|a Antigens, CD
|2 NLM
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|a B7-1 Antigen
|2 NLM
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|a CD11a Antigen
|2 NLM
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|a CD28 Antigens
|2 NLM
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|a CD3 Complex
|2 NLM
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|a CD58 Antigens
|2 NLM
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|a ICOSLG protein, human
|2 NLM
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|a IL10 protein, human
|2 NLM
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|a IL4 protein, human
|2 NLM
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|a Immunoconjugates
|2 NLM
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|a Immunosuppressive Agents
|2 NLM
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|a Inducible T-Cell Co-Stimulator Ligand
|2 NLM
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|a Interleukin-2
|2 NLM
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|a Lymphocyte Function-Associated Antigen-1
|2 NLM
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|a Intercellular Adhesion Molecule-1
|2 NLM
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|a 126547-89-5
|2 NLM
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|a Interleukin-10
|2 NLM
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|a 130068-27-8
|2 NLM
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7 |
|a Interleukin-4
|2 NLM
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|a 207137-56-2
|2 NLM
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|a Abatacept
|2 NLM
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|a 7D0YB67S97
|2 NLM
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|a Interferon-gamma
|2 NLM
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|a 82115-62-6
|2 NLM
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|a efalizumab
|2 NLM
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|a XX2MN88N5D
|2 NLM
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1 |
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|a Leitner, Judith
|e verfasserin
|4 aut
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1 |
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|a Majdic, Otto
|e verfasserin
|4 aut
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1 |
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|a Pickl, Winfried F
|e verfasserin
|4 aut
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1 |
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|a Zlabinger, Gerhard J
|e verfasserin
|4 aut
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1 |
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|a Grabmeier-Pfistershammer, Katharina
|e verfasserin
|4 aut
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1 |
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|a Steinberger, Peter
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 139(2011), 2 vom: 15. Mai, Seite 199-207
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:139
|g year:2011
|g number:2
|g day:15
|g month:05
|g pages:199-207
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|u http://dx.doi.org/10.1016/j.clim.2011.02.007
|3 Volltext
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|a AR
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|d 139
|j 2011
|e 2
|b 15
|c 05
|h 199-207
|