IL-4 enhances keratinocyte expression of CXCR3 agonistic chemokines

Cristina Albanesi, Claudia Scarponi, Silvia Sebastiani, Andrea Cavani, Monica Federici, Ornella De Pità, Pietro Puddu, Giampiero Girolomoni

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Abstract

IFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-γ (Mig), and IFN-inducible T-cell α-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-γ or TNF-α-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- γ and IL-4 and expressed moderate to high levels of CXCR3. Finally, CXCR3 agonistic chemokines released by stimulated keratinocytes triggered calcium mobilization in skin-derived nickel-specific CD4+ T cells and promoted their migration, with supernatant from keratinocyte cultures stimulated with IFN-γ and IL-4 attracting more efficaciously than supernatant from keratinocytes activated with IFN-γ alone. In conclusion, IL-4 exerts a proinflammatory function on keratinocytes by potentiating IFN-γ and TNF-α induction of IP- 10, Mig, and I-TAC, which in turn may determine a prominent recruitment of CXCR3+ T lymphocytes at inflammatory reaction sites.

Original languageEnglish
Pages (from-to)1395-1402
Number of pages8
JournalJournal of Immunology
Volume165
Issue number3
Publication statusPublished - Aug 1 2000

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Keratinocytes
Chemokines
Interleukin-4
T-Lymphocytes
Chemotactic Factors
Allergic Contact Dermatitis
Interleukin-17
Nickel
arginine glutamate
Interleukin-10
Skin
CXCR3 Receptors
Monokines
CXC Chemokines
Leucine
Immunohistochemistry
Staining and Labeling
Cytokines
Calcium
Cell Line

ASJC Scopus subject areas

  • Immunology

Cite this

Albanesi, C., Scarponi, C., Sebastiani, S., Cavani, A., Federici, M., De Pità, O., ... Girolomoni, G. (2000). IL-4 enhances keratinocyte expression of CXCR3 agonistic chemokines. Journal of Immunology, 165(3), 1395-1402.

IL-4 enhances keratinocyte expression of CXCR3 agonistic chemokines. / Albanesi, Cristina; Scarponi, Claudia; Sebastiani, Silvia; Cavani, Andrea; Federici, Monica; De Pità, Ornella; Puddu, Pietro; Girolomoni, Giampiero.

In: Journal of Immunology, Vol. 165, No. 3, 01.08.2000, p. 1395-1402.

Research output: Contribution to journalArticle

Albanesi, C, Scarponi, C, Sebastiani, S, Cavani, A, Federici, M, De Pità, O, Puddu, P & Girolomoni, G 2000, 'IL-4 enhances keratinocyte expression of CXCR3 agonistic chemokines', Journal of Immunology, vol. 165, no. 3, pp. 1395-1402.
Albanesi C, Scarponi C, Sebastiani S, Cavani A, Federici M, De Pità O et al. IL-4 enhances keratinocyte expression of CXCR3 agonistic chemokines. Journal of Immunology. 2000 Aug 1;165(3):1395-1402.
Albanesi, Cristina ; Scarponi, Claudia ; Sebastiani, Silvia ; Cavani, Andrea ; Federici, Monica ; De Pità, Ornella ; Puddu, Pietro ; Girolomoni, Giampiero. / IL-4 enhances keratinocyte expression of CXCR3 agonistic chemokines. In: Journal of Immunology. 2000 ; Vol. 165, No. 3. pp. 1395-1402.
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abstract = "IFN-induced protein of 10 kDa (IP-10), monokine induced by IFN-γ (Mig), and IFN-inducible T-cell α-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-γ or TNF-α-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- γ and IL-4 and expressed moderate to high levels of CXCR3. Finally, CXCR3 agonistic chemokines released by stimulated keratinocytes triggered calcium mobilization in skin-derived nickel-specific CD4+ T cells and promoted their migration, with supernatant from keratinocyte cultures stimulated with IFN-γ and IL-4 attracting more efficaciously than supernatant from keratinocytes activated with IFN-γ alone. In conclusion, IL-4 exerts a proinflammatory function on keratinocytes by potentiating IFN-γ and TNF-α induction of IP- 10, Mig, and I-TAC, which in turn may determine a prominent recruitment of CXCR3+ T lymphocytes at inflammatory reaction sites.",
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AU - De Pità, Ornella

AU - Puddu, Pietro

AU - Girolomoni, Giampiero

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