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IL-4 enhances keratinocyte expression of CXCR3 agonistic chemokines

IFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T-cell alpha-chemoattractant (I-TAC) belong to the non-glutamate-leucine-arginine motif CXC chemokine family and act solely through the CXCR3 receptor for potent attraction of T lymphocytes. In this study,... Full description

Journal Title: Journal of immunology (Baltimore Md. : 1950), 01 August 2000, Vol.165(3), pp.1395-402
Main Author: Albanesi, C
Other Authors: Scarponi, C , Sebastiani, S , Cavani, A , Federici, M , De Pità, O , Puddu, P , Girolomoni, G
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0022-1767 ; PMID: 10903743 Version:1
Link: http://pubmed.gov/10903743
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recordid: medline10903743
title: IL-4 enhances keratinocyte expression of CXCR3 agonistic chemokines
format: Article
creator:
  • Albanesi, C
  • Scarponi, C
  • Sebastiani, S
  • Cavani, A
  • Federici, M
  • De Pità, O
  • Puddu, P
  • Girolomoni, G
subjects:
  • Intercellular Signaling Peptides and Proteins
  • Adjuvants, Immunologic -- Physiology
  • Interleukin-4 -- Physiology
  • Keratinocytes -- Immunology
  • Receptors, Chemokine -- Agonists
ispartof: Journal of immunology (Baltimore, Md. : 1950), 01 August 2000, Vol.165(3), pp.1395-402
description: IFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T-cell alpha-chemoattractant (I-TAC) belong to the non-glutamate-leucine-arginine motif CXC chemokine family and act solely through the CXCR3 receptor for potent attraction of T lymphocytes. In this study, we evaluated the capacity of the T cell-derived cytokines IL-4, IL-10, and IL-17 to modulate IP-10, Mig, and I-TAC in cultured human keratinocytes and CXCR3 expression in T cells from allergic contact dermatitis (ACD). IL-4, but not IL-10 or IL-17, significantly up-regulated IFN-gamma- or TNF-alpha-induced IP-10, Mig, and I-TAC mRNA accumulation in keratinocytes and increased the levels of IP-10 and Mig in keratinocyte supernatants. Immunohistochemistry of skin affected by ACD revealed that >70% of infiltrating cells were reactive for CXCR3 and that CXCR3 staining colocalized in CD4+ and CD8+ T cells. Nickel-specific CD4+ and CD8+ T cell lines established from ACD skin produced IFN-gamma and...
language: eng
source:
identifier: ISSN: 0022-1767 ; PMID: 10903743 Version:1
fulltext: fulltext
issn:
  • 00221767
  • 0022-1767
url: Link


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titleIL-4 enhances keratinocyte expression of CXCR3 agonistic chemokines
creatorAlbanesi, C ; Scarponi, C ; Sebastiani, S ; Cavani, A ; Federici, M ; De Pità, O ; Puddu, P ; Girolomoni, G
ispartofJournal of immunology (Baltimore, Md. : 1950), 01 August 2000, Vol.165(3), pp.1395-402
identifierISSN: 0022-1767 ; PMID: 10903743 Version:1
subjectIntercellular Signaling Peptides and Proteins ; Adjuvants, Immunologic -- Physiology ; Interleukin-4 -- Physiology ; Keratinocytes -- Immunology ; Receptors, Chemokine -- Agonists
descriptionIFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T-cell alpha-chemoattractant (I-TAC) belong to the non-glutamate-leucine-arginine motif CXC chemokine family and act solely through the CXCR3 receptor for potent attraction of T lymphocytes. In this study, we evaluated the capacity of the T cell-derived cytokines IL-4, IL-10, and IL-17 to modulate IP-10, Mig, and I-TAC in cultured human keratinocytes and CXCR3 expression in T cells from allergic contact dermatitis (ACD). IL-4, but not IL-10 or IL-17, significantly up-regulated IFN-gamma- or TNF-alpha-induced IP-10, Mig, and I-TAC mRNA accumulation in keratinocytes and increased the levels of IP-10 and Mig in keratinocyte supernatants. Immunohistochemistry of skin affected by ACD revealed that >70% of infiltrating cells were reactive for CXCR3 and that CXCR3 staining colocalized in CD4+ and CD8+ T cells. Nickel-specific CD4+ and CD8+ T cell lines established from ACD skin produced IFN-gamma and...
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titleIL-4 enhances keratinocyte expression of CXCR3 agonistic chemokines
descriptionIFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T-cell alpha-chemoattractant (I-TAC) belong to the non-glutamate-leucine-arginine motif CXC chemokine family and act solely through the CXCR3 receptor for potent attraction of T lymphocytes. In this study, we evaluated the capacity of the T cell-derived cytokines IL-4, IL-10, and IL-17 to modulate IP-10, Mig, and I-TAC in cultured human keratinocytes and CXCR3 expression in T cells from allergic contact dermatitis (ACD). IL-4, but not IL-10 or IL-17, significantly up-regulated IFN-gamma- or TNF-alpha-induced IP-10, Mig, and I-TAC mRNA accumulation in keratinocytes and increased the levels of IP-10 and Mig in keratinocyte supernatants. Immunohistochemistry of skin affected by ACD revealed that >70% of infiltrating cells were reactive for CXCR3 and that CXCR3 staining colocalized in CD4+ and CD8+ T cells. Nickel-specific CD4+ and CD8+ T cell lines established from ACD skin produced IFN-gamma and...
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abstractIFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T-cell alpha-chemoattractant (I-TAC) belong to the non-glutamate-leucine-arginine motif CXC chemokine family and act solely through the CXCR3 receptor for potent attraction of T lymphocytes. In this study, we evaluated the capacity of the T cell-derived cytokines IL-4, IL-10, and IL-17 to modulate IP-10, Mig, and I-TAC in cultured human keratinocytes and CXCR3 expression in T cells from allergic contact dermatitis (ACD). IL-4, but not IL-10 or IL-17, significantly up-regulated IFN-gamma- or TNF-alpha-induced IP-10, Mig, and I-TAC mRNA accumulation in keratinocytes and increased the levels of IP-10 and Mig in keratinocyte supernatants. Immunohistochemistry of skin affected by ACD revealed that >70% of infiltrating cells were reactive for CXCR3 and that CXCR3 staining colocalized in CD4+ and CD8+ T cells. Nickel-specific CD4+ and CD8+ T cell lines established from ACD skin produced IFN-gamma and...
pmid10903743
doi10.4049/jimmunol.165.3.1395
eissn15506606
date2000-08-01