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231223s2008 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2007.12.004
|2 doi
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|a pubmed24n0593.xml
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|a (DE-627)NLM177985461
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|a (NLM)18313361
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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 Capraru, Dorin
|e verfasserin
|4 aut
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|a Expansion of circulating NKG2D+ effector memory T-cells and expression of NKG2D-ligand MIC in granulomaous lesions in Wegener's granulomatosis
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|c 2008
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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 24.06.2008
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|a Date Revised 16.11.2017
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Expansion of circulating CD28- T-cells reminiscent of effector memory T-cells (T(EM)) has been reported in Wegener's granulomatosis (WG) recently. To investigate the role of T(EM) in WG, we analyzed the expression of the activating NK-receptor NKG2D and its ligand MIC on circulating T(EM) and in granulomatous lesions, respectively. NKG2D was anomalously expressed and preferentially detected on circulating CD4+CD28- T(EM) in WG. Compared to healthy controls, T(EM) display a more activated phenotype potentially favoring unbalanced proinflammatory responses in WG. Cluster-like formations of "Wegener's autoantigen" PR3 were surrounded by NKG2D+ and NKG2D-ligand MIC+ cells in WG-granulomata, but not in disease controls. Further, IL-15 - known to drive T(EM) differentiation and proliferation--was also expressed in WG-granulomata. Thus, through acquisition of NK-like "innate" properties, IL-15 stimulated NKG2D+ T(EM) could interact with MIC+ cells within WG-granulomata, thereby sustaining inflammation and autoimmunity and promoting self-perpetuating pathology in WG
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a CD28 Antigens
|2 NLM
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|a GPI-Linked Proteins
|2 NLM
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|a Intercellular Signaling Peptides and Proteins
|2 NLM
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|a Interleukin-15
|2 NLM
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|a KLRK1 protein, human
|2 NLM
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|a NK Cell Lectin-Like Receptor Subfamily K
|2 NLM
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|a Receptors, Immunologic
|2 NLM
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|a Receptors, Natural Killer Cell
|2 NLM
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|a ULBP2 protein, human
|2 NLM
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|a Myeloblastin
|2 NLM
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|a EC 3.4.21.76
|2 NLM
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1 |
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|a Müller, Antje
|e verfasserin
|4 aut
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1 |
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|a Csernok, Elena
|e verfasserin
|4 aut
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1 |
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|a Gross, Wolfgang L
|e verfasserin
|4 aut
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1 |
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|a Holl-Ulrich, Konstanze
|e verfasserin
|4 aut
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1 |
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|a Northfield, John
|e verfasserin
|4 aut
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1 |
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|a Klenerman, Paul
|e verfasserin
|4 aut
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1 |
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|a Herlyn, Karen
|e verfasserin
|4 aut
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1 |
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|a Holle, Julia
|e verfasserin
|4 aut
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1 |
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|a Gottschlich, Stefan
|e verfasserin
|4 aut
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1 |
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|a Voswinkel, Jan
|e verfasserin
|4 aut
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1 |
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|a Spies, Thomas
|e verfasserin
|4 aut
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1 |
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|a Fagin, Ursula
|e verfasserin
|4 aut
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1 |
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|a Jabs, Wolfram J
|e verfasserin
|4 aut
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1 |
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|a Lamprecht, Peter
|e verfasserin
|4 aut
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773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 127(2008), 2 vom: 15. Mai, Seite 144-50
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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1 |
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|g volume:127
|g year:2008
|g number:2
|g day:15
|g month:05
|g pages:144-50
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|u http://dx.doi.org/10.1016/j.clim.2007.12.004
|3 Volltext
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|a GBV_USEFLAG_A
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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 127
|j 2008
|e 2
|b 15
|c 05
|h 144-50
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