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231222s2003 xx ||||| 00| ||eng c |
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|a pubmed24n0423.xml
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|a (DE-627)NLM126744688
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|a (NLM)12921754
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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100 |
1 |
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|a Kepley, Christopher L
|e verfasserin
|4 aut
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245 |
1 |
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|a FcepsilonRI-FcgammaRII coaggregation inhibits IL-16 production from human Langerhans-like dendritic cells
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|c 2003
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336 |
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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 01.10.2003
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|a Date Revised 07.11.2019
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|a published: Print
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|a Citation Status MEDLINE
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|a Langerhans-like dendritic cells (LLDC) express the high-affinity IgE receptor FcepsilonRI form that lacks the beta-chain, and may play an important role in allergic inflammation via production of IL-16. Secretion of mediators by human mast cells and basophils is mediated through FcepsilonRI and is decreased by coaggregating these receptors to the low-affinity IgG receptor, FcgammaRII. We used a recently described human Ig fusion protein (GE2), which is composed of key portions of the human gamma1 and the human epsilon heavy chains, to investigate its ability to inhibit IL-16 production from FcepsilonRI-positive Langerhans-like dendritic cells through coaggregation of FcgammaRII and FcepsilonRI. Unstimulated LLDC-derived from CD14-positive monocytes from atopic donors were shown to express FcgammaRII, an ITIM-containing receptor, but not FcepsilonRI or FcgammaRIII which are activating (ITAM) receptors. When passively sensitized with antigen-specific, human IgE and then challenged with antigen, LLDC were stimulated to produce IL-16. However, when FcepsilonRI and FcgammaRII were coaggregated with GE2, IL-16 production was significantly inhibited. Exposure of LLDCs to GE2 alone did not induce IL-16 production. Our results further extend our studies demonstrating the ability of GE2 to inhibit FcepsilonRI-mediated responses through coaggregation with FcgammaRIIB and at the same time show that human LDCC can be modulated in a fashion similar to mast cells and basophils
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4 |
|a Journal Article
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4 |
|a Research Support, Non-U.S. Gov't
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650 |
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|a Research Support, U.S. Gov't, P.H.S.
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650 |
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|a FCGR2A protein, human
|2 NLM
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650 |
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7 |
|a FCGR2B protein, human
|2 NLM
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650 |
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7 |
|a Interleukin-16
|2 NLM
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7 |
|a Receptors, IgE
|2 NLM
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7 |
|a Receptors, IgG
|2 NLM
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700 |
1 |
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|a Zhang, Ke
|e verfasserin
|4 aut
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700 |
1 |
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|a Zhu, Daocheng
|e verfasserin
|4 aut
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700 |
1 |
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|a Saxon, Andrew
|e verfasserin
|4 aut
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773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 108(2003), 2 vom: 15. Aug., Seite 89-94
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
1 |
8 |
|g volume:108
|g year:2003
|g number:2
|g day:15
|g month:08
|g pages:89-94
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912 |
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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912 |
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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 108
|j 2003
|e 2
|b 15
|c 08
|h 89-94
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