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231225s2018 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2017.10.004
|2 doi
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|a pubmed24n0923.xml
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|a (DE-627)NLM277003636
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|a (NLM)29031579
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|a (PII)S1521-6616(17)30567-3
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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 Umeda, Masataka
|e verfasserin
|4 aut
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|a CD4+ CD52lo T-cell expression contributes to the development of systemic lupus erythematosus
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|c 2018
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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 18.03.2019
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|a Date Revised 18.03.2019
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2017 Elsevier Inc. All rights reserved.
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|a The cell-surface glycoprotein CD52 is widely expressed in lymphocytes. CD4+CD52hi T cells are functioning suppressor CD4+T cells. We investigated the role of the immune regulation of CD4+CD52 T cells in systemic lupus erythematosus (SLE). CD4+CD52lo T cells were increased in SLE patients, in positive correlation with SLEDAI, anti-ds-DNA antibody, and IgG concentration. Circulating follicular helper-like T cells (Tfh-like cells) were also increased in SLE, in positive correlation with CD4+CD52lo T cells. Chemokine receptor 8 (CCR8) expression in CD4+CD52lo T cells was increased. In vitro experiments using CD4 T cells of SLE patients showed that thymus and activation-regulated chemokine (TARC), a ligand of CCR8, contributed to the development of CD4+CD52hi T cells into CD4+CD52lo T cells. Our findings suggest that CD4+CD52lo T-cell upregulation is involved in the production of pathogens by autoantibodies, and TARC may contribute to the development of SLE through an aberrant induction of CD4+CD52lo T cells
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a CD52
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|a Systemic lupus erythematosus
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|a T cells
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|a Antibodies, Antinuclear
|2 NLM
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|a Autoantibodies
|2 NLM
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|a CCL17 protein, human
|2 NLM
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|a CCR8 protein, human
|2 NLM
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|a CD52 Antigen
|2 NLM
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|a CD52 protein, human
|2 NLM
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|a Chemokine CCL17
|2 NLM
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|a Immunoglobulin G
|2 NLM
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|a Receptors, CCR8
|2 NLM
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|a Koga, Tomohiro
|e verfasserin
|4 aut
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|a Ichinose, Kunihiro
|e verfasserin
|4 aut
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|a Igawa, Takashi
|e verfasserin
|4 aut
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|a Sato, Tomohito
|e verfasserin
|4 aut
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|a Takatani, Ayuko
|e verfasserin
|4 aut
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|a Shimizu, Toshimasa
|e verfasserin
|4 aut
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|a Fukui, Shoichi
|e verfasserin
|4 aut
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|a Nishino, Ayako
|e verfasserin
|4 aut
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|a Horai, Yoshiro
|e verfasserin
|4 aut
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|a Hirai, Yasuko
|e verfasserin
|4 aut
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|a Kawashiri, Shin-Ya
|e verfasserin
|4 aut
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|a Iwamoto, Naoki
|e verfasserin
|4 aut
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|a Aramaki, Toshiyuki
|e verfasserin
|4 aut
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|a Tamai, Mami
|e verfasserin
|4 aut
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|a Nakamura, Hideki
|e verfasserin
|4 aut
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|a Yamamoto, Kazuo
|e verfasserin
|4 aut
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|a Abiru, Norio
|e verfasserin
|4 aut
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|a Origuchi, Tomoki
|e verfasserin
|4 aut
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|a Ueki, Yukitaka
|e verfasserin
|4 aut
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|a Kawakami, Atsushi
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 187(2018) vom: 01. Feb., Seite 50-57
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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|g volume:187
|g year:2018
|g day:01
|g month:02
|g pages:50-57
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|u http://dx.doi.org/10.1016/j.clim.2017.10.004
|3 Volltext
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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 187
|j 2018
|b 01
|c 02
|h 50-57
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