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231224s2017 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2016.10.011
|2 doi
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| 028 |
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2 |
|a pubmed24n0890.xml
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|a (DE-627)NLM267249446
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|a (NLM)27989899
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|a (PII)S1521-6616(16)30160-7
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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 Tabor, Dana E
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a Estrogen receptor alpha promotes lupus in (NZB×NZW)F1 mice in a B cell intrinsic manner
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| 264 |
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1 |
|c 2017
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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 ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 13.06.2017
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|a Date Revised 13.11.2018
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|a published: Print-Electronic
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|a CommentIn: Nat Rev Nephrol. 2017 Jan;13(1):2. - PMID 27840420
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| 500 |
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|a Citation Status MEDLINE
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| 520 |
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|a Copyright © 2016 Elsevier Inc. All rights reserved.
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|a Lupus is a systemic autoimmune disease characterized by the production of autoreactive antibodies against nuclear antigens. Women are disproportionately affected by lupus, and this sex bias is thought to be due, in large part, to the ability of estrogens to promote lupus pathogenesis. Previously, we have shown that global deletion of estrogen receptor alpha (ERα) significantly attenuated loss of tolerance, immune cell activation, autoantibody production, and the development of lupus nephritis. Here we show that targeted deletion of ERα specifically in B cells retards production of pathogenic autoantibodies and the development of nephritis in lupus-prone (NZB×NZW)F1 mice. Furthermore, we observed that ERα deletion in B cells was associated with decreased B cell activation in young, pre-autoimmune (NZB×NZW)F1 females. Altogether, these data suggest that ERα acts in a B cell-intrinsic manner to control B cell activation, autoantibody production, and lupus nephritis
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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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4 |
|a Research Support, N.I.H., Extramural
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| 650 |
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4 |
|a B cell
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| 650 |
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4 |
|a Estrogen receptor alpha
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| 650 |
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4 |
|a Immune cell activation
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| 650 |
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4 |
|a Immunologic tolerance
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| 650 |
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4 |
|a Lupus
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| 650 |
|
7 |
|a Antibodies, Antinuclear
|2 NLM
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| 650 |
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7 |
|a Antigens, CD19
|2 NLM
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| 650 |
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7 |
|a CD19 antigen, mouse
|2 NLM
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| 650 |
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7 |
|a Estrogen Receptor alpha
|2 NLM
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| 650 |
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7 |
|a Immunoglobulin G
|2 NLM
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| 650 |
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7 |
|a Cre recombinase
|2 NLM
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| 650 |
|
7 |
|a EC 2.7.7.-
|2 NLM
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| 650 |
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7 |
|a Integrases
|2 NLM
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| 650 |
|
7 |
|a EC 2.7.7.-
|2 NLM
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| 700 |
1 |
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|a Gould, Karen A
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 174(2017) vom: 28. Jan., Seite 41-52
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:174
|g year:2017
|g day:28
|g month:01
|g pages:41-52
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| 856 |
4 |
0 |
|u http://dx.doi.org/10.1016/j.clim.2016.10.011
|3 Volltext
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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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| 912 |
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|a GBV_ILN_11
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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 174
|j 2017
|b 28
|c 01
|h 41-52
|