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Data on the expression of CXCR3 ligands and pro-inflammatory cytokines in macrophages and CD4(+) T cells after stimuli of CXCR3 ligands

C-X-C motif chemokine receptor 3 (CXCR3) is a G protein-coupled receptor for three ligands which are C-X-C motif chemokine 9 (CXCL9), CXCL10, and CXCL11 [1]. Previously we have reported that CXCL10 promotes pro-inflammatory cytokine expression, and forms positive feedback loop [2], [3]. In the prese...

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Autores principales: Kim, Bongjun, Lee, Jong-Ho, Jin, Won Jong, Kim, Hong-Hee, Ha, Hyunil, Lee, Zang Hee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5996269/
https://www.ncbi.nlm.nih.gov/pubmed/29900211
http://dx.doi.org/10.1016/j.dib.2018.03.042
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author Kim, Bongjun
Lee, Jong-Ho
Jin, Won Jong
Kim, Hong-Hee
Ha, Hyunil
Lee, Zang Hee
author_facet Kim, Bongjun
Lee, Jong-Ho
Jin, Won Jong
Kim, Hong-Hee
Ha, Hyunil
Lee, Zang Hee
author_sort Kim, Bongjun
collection PubMed
description C-X-C motif chemokine receptor 3 (CXCR3) is a G protein-coupled receptor for three ligands which are C-X-C motif chemokine 9 (CXCL9), CXCL10, and CXCL11 [1]. Previously we have reported that CXCL10 promotes pro-inflammatory cytokine expression, and forms positive feedback loop [2], [3]. In the present study, we described mRNA expression of CXCL9 and CXCL11 under CXCL10 stimuli in the presence or absence of CXCR3 antagonist, JN-2 in bone marrow-derived macrophages (BMMs) and CD4(+) T cells. In addition, we examined pro-inflammatory cytokine expression under CXCL9 or CXCL11 stimuli in BMMs and CD4(+) T cells.
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spelling pubmed-59962692018-06-13 Data on the expression of CXCR3 ligands and pro-inflammatory cytokines in macrophages and CD4(+) T cells after stimuli of CXCR3 ligands Kim, Bongjun Lee, Jong-Ho Jin, Won Jong Kim, Hong-Hee Ha, Hyunil Lee, Zang Hee Data Brief Cell biology    C-X-C motif chemokine receptor 3 (CXCR3) is a G protein-coupled receptor for three ligands which are C-X-C motif chemokine 9 (CXCL9), CXCL10, and CXCL11 [1]. Previously we have reported that CXCL10 promotes pro-inflammatory cytokine expression, and forms positive feedback loop [2], [3]. In the present study, we described mRNA expression of CXCL9 and CXCL11 under CXCL10 stimuli in the presence or absence of CXCR3 antagonist, JN-2 in bone marrow-derived macrophages (BMMs) and CD4(+) T cells. In addition, we examined pro-inflammatory cytokine expression under CXCL9 or CXCL11 stimuli in BMMs and CD4(+) T cells. Elsevier 2018-03-15 /pmc/articles/PMC5996269/ /pubmed/29900211 http://dx.doi.org/10.1016/j.dib.2018.03.042 Text en © 2018 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Cell biology   
Kim, Bongjun
Lee, Jong-Ho
Jin, Won Jong
Kim, Hong-Hee
Ha, Hyunil
Lee, Zang Hee
Data on the expression of CXCR3 ligands and pro-inflammatory cytokines in macrophages and CD4(+) T cells after stimuli of CXCR3 ligands
title Data on the expression of CXCR3 ligands and pro-inflammatory cytokines in macrophages and CD4(+) T cells after stimuli of CXCR3 ligands
title_full Data on the expression of CXCR3 ligands and pro-inflammatory cytokines in macrophages and CD4(+) T cells after stimuli of CXCR3 ligands
title_fullStr Data on the expression of CXCR3 ligands and pro-inflammatory cytokines in macrophages and CD4(+) T cells after stimuli of CXCR3 ligands
title_full_unstemmed Data on the expression of CXCR3 ligands and pro-inflammatory cytokines in macrophages and CD4(+) T cells after stimuli of CXCR3 ligands
title_short Data on the expression of CXCR3 ligands and pro-inflammatory cytokines in macrophages and CD4(+) T cells after stimuli of CXCR3 ligands
title_sort data on the expression of cxcr3 ligands and pro-inflammatory cytokines in macrophages and cd4(+) t cells after stimuli of cxcr3 ligands
topic Cell biology   
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5996269/
https://www.ncbi.nlm.nih.gov/pubmed/29900211
http://dx.doi.org/10.1016/j.dib.2018.03.042
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