Macrophage migration inhibitory factor triggers chemotaxis of CD74+CXCR2+NKT cells in chemically induced IFN-γ-Mediated skin inflammation

Chia-Yuan Hsieh, Chia-Ling Chen, Yee-Shin Lin, Trai-Ming Yeh, Tsung-Ting Tsai, Ming-Yuan Hong, Chiou Feng Lin

研究成果: 雜誌貢獻文章

13 引文 (Scopus)

摘要

IFN-γ mediates chemically induced skin inflammation; however, the mechanism by which IFN-γ-producing cells are recruited to the sites of inflammation remains undefined. Secretion of macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, from damaged cells may promote immune cell recruitment. We hypothesized that MIF triggers an initial step in the chemotaxis of IFN-γ-producing cells in chemically induced skin inflammation. Using acute and chronic models of 12-Otetradecanoylphorbol- 13-acetate (TPA)-induced skin inflammation in mouse ears, MIF expression was examined, and its role in this process was investigated pharmacologically. The cell populations targeted by MIF, their receptor expression patterns, and the effects of MIF on cell migration were examined. TPA directly caused cytotoxicity accompanied by MIF release in mouse ear epidermal keratinocytes, as well as in human keratinocytic HaCaT cells. Treatment with theMIF antagonist (S,R)-3-(4-hydroxyphenyl)- 4,5-dihydro-5-isoxazole acetic acid methyl ester considerably attenuated TPA-induced ear swelling, leukocyte infiltration, epidermal cell proliferation, and dermal angiogenesis. Inhibition of MIF greatly diminished the dermal infiltration of IFN-γ+ NKT cells, whereas the addition of exogenous TPA and MIF to NKT cells promoted their IFN-γ production and migration, respectively. MIF specifically triggered the chemotaxis of NKT cells via CD74 and CXCR2, and the resulting depletion of NKT cells abolished TPAinduced skin inflammation. In TPA-induced skin inflammation, MIF is released from damaged keratinocytes and then triggers the chemotaxis of CD74+CXCR2+ NKT cells for IFN-γ production.
原文英語
頁(從 - 到)3693-3703
頁數11
期刊Journal of Immunology
193
發行號7
DOIs
出版狀態已發佈 - 十月 1 2014

指紋

Macrophage Migration-Inhibitory Factors
Natural Killer T-Cells
Chemotaxis
Inflammation
Skin
Acetates
Ear
Keratinocytes
Isoxazoles
Cell Movement
Leukocytes
Cell Proliferation
Cytokines

ASJC Scopus subject areas

  • Immunology
  • Medicine(all)

引用此文

Macrophage migration inhibitory factor triggers chemotaxis of CD74+CXCR2+NKT cells in chemically induced IFN-γ-Mediated skin inflammation. / Hsieh, Chia-Yuan; Chen, Chia-Ling; Lin, Yee-Shin; Yeh, Trai-Ming; Tsai, Tsung-Ting; Hong, Ming-Yuan; Lin, Chiou Feng.

於: Journal of Immunology, 卷 193, 編號 7, 01.10.2014, p. 3693-3703.

研究成果: 雜誌貢獻文章

Hsieh, Chia-Yuan ; Chen, Chia-Ling ; Lin, Yee-Shin ; Yeh, Trai-Ming ; Tsai, Tsung-Ting ; Hong, Ming-Yuan ; Lin, Chiou Feng. / Macrophage migration inhibitory factor triggers chemotaxis of CD74+CXCR2+NKT cells in chemically induced IFN-γ-Mediated skin inflammation. 於: Journal of Immunology. 2014 ; 卷 193, 編號 7. 頁 3693-3703.
@article{39e5fd72ac5140359e4f8653e2da0d90,
title = "Macrophage migration inhibitory factor triggers chemotaxis of CD74+CXCR2+NKT cells in chemically induced IFN-γ-Mediated skin inflammation",
abstract = "IFN-γ mediates chemically induced skin inflammation; however, the mechanism by which IFN-γ-producing cells are recruited to the sites of inflammation remains undefined. Secretion of macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, from damaged cells may promote immune cell recruitment. We hypothesized that MIF triggers an initial step in the chemotaxis of IFN-γ-producing cells in chemically induced skin inflammation. Using acute and chronic models of 12-Otetradecanoylphorbol- 13-acetate (TPA)-induced skin inflammation in mouse ears, MIF expression was examined, and its role in this process was investigated pharmacologically. The cell populations targeted by MIF, their receptor expression patterns, and the effects of MIF on cell migration were examined. TPA directly caused cytotoxicity accompanied by MIF release in mouse ear epidermal keratinocytes, as well as in human keratinocytic HaCaT cells. Treatment with theMIF antagonist (S,R)-3-(4-hydroxyphenyl)- 4,5-dihydro-5-isoxazole acetic acid methyl ester considerably attenuated TPA-induced ear swelling, leukocyte infiltration, epidermal cell proliferation, and dermal angiogenesis. Inhibition of MIF greatly diminished the dermal infiltration of IFN-γ+ NKT cells, whereas the addition of exogenous TPA and MIF to NKT cells promoted their IFN-γ production and migration, respectively. MIF specifically triggered the chemotaxis of NKT cells via CD74 and CXCR2, and the resulting depletion of NKT cells abolished TPAinduced skin inflammation. In TPA-induced skin inflammation, MIF is released from damaged keratinocytes and then triggers the chemotaxis of CD74+CXCR2+ NKT cells for IFN-γ production.",
author = "Chia-Yuan Hsieh and Chia-Ling Chen and Yee-Shin Lin and Trai-Ming Yeh and Tsung-Ting Tsai and Ming-Yuan Hong and Lin, {Chiou Feng}",
year = "2014",
month = "10",
day = "1",
doi = "10.4049/jimmunol.1400692",
language = "English",
volume = "193",
pages = "3693--3703",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "7",

}

TY - JOUR

T1 - Macrophage migration inhibitory factor triggers chemotaxis of CD74+CXCR2+NKT cells in chemically induced IFN-γ-Mediated skin inflammation

AU - Hsieh, Chia-Yuan

AU - Chen, Chia-Ling

AU - Lin, Yee-Shin

AU - Yeh, Trai-Ming

AU - Tsai, Tsung-Ting

AU - Hong, Ming-Yuan

AU - Lin, Chiou Feng

PY - 2014/10/1

Y1 - 2014/10/1

N2 - IFN-γ mediates chemically induced skin inflammation; however, the mechanism by which IFN-γ-producing cells are recruited to the sites of inflammation remains undefined. Secretion of macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, from damaged cells may promote immune cell recruitment. We hypothesized that MIF triggers an initial step in the chemotaxis of IFN-γ-producing cells in chemically induced skin inflammation. Using acute and chronic models of 12-Otetradecanoylphorbol- 13-acetate (TPA)-induced skin inflammation in mouse ears, MIF expression was examined, and its role in this process was investigated pharmacologically. The cell populations targeted by MIF, their receptor expression patterns, and the effects of MIF on cell migration were examined. TPA directly caused cytotoxicity accompanied by MIF release in mouse ear epidermal keratinocytes, as well as in human keratinocytic HaCaT cells. Treatment with theMIF antagonist (S,R)-3-(4-hydroxyphenyl)- 4,5-dihydro-5-isoxazole acetic acid methyl ester considerably attenuated TPA-induced ear swelling, leukocyte infiltration, epidermal cell proliferation, and dermal angiogenesis. Inhibition of MIF greatly diminished the dermal infiltration of IFN-γ+ NKT cells, whereas the addition of exogenous TPA and MIF to NKT cells promoted their IFN-γ production and migration, respectively. MIF specifically triggered the chemotaxis of NKT cells via CD74 and CXCR2, and the resulting depletion of NKT cells abolished TPAinduced skin inflammation. In TPA-induced skin inflammation, MIF is released from damaged keratinocytes and then triggers the chemotaxis of CD74+CXCR2+ NKT cells for IFN-γ production.

AB - IFN-γ mediates chemically induced skin inflammation; however, the mechanism by which IFN-γ-producing cells are recruited to the sites of inflammation remains undefined. Secretion of macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, from damaged cells may promote immune cell recruitment. We hypothesized that MIF triggers an initial step in the chemotaxis of IFN-γ-producing cells in chemically induced skin inflammation. Using acute and chronic models of 12-Otetradecanoylphorbol- 13-acetate (TPA)-induced skin inflammation in mouse ears, MIF expression was examined, and its role in this process was investigated pharmacologically. The cell populations targeted by MIF, their receptor expression patterns, and the effects of MIF on cell migration were examined. TPA directly caused cytotoxicity accompanied by MIF release in mouse ear epidermal keratinocytes, as well as in human keratinocytic HaCaT cells. Treatment with theMIF antagonist (S,R)-3-(4-hydroxyphenyl)- 4,5-dihydro-5-isoxazole acetic acid methyl ester considerably attenuated TPA-induced ear swelling, leukocyte infiltration, epidermal cell proliferation, and dermal angiogenesis. Inhibition of MIF greatly diminished the dermal infiltration of IFN-γ+ NKT cells, whereas the addition of exogenous TPA and MIF to NKT cells promoted their IFN-γ production and migration, respectively. MIF specifically triggered the chemotaxis of NKT cells via CD74 and CXCR2, and the resulting depletion of NKT cells abolished TPAinduced skin inflammation. In TPA-induced skin inflammation, MIF is released from damaged keratinocytes and then triggers the chemotaxis of CD74+CXCR2+ NKT cells for IFN-γ production.

UR - http://www.scopus.com/inward/record.url?scp=84907200174&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84907200174&partnerID=8YFLogxK

U2 - 10.4049/jimmunol.1400692

DO - 10.4049/jimmunol.1400692

M3 - Article

C2 - 25172501

AN - SCOPUS:84907200174

VL - 193

SP - 3693

EP - 3703

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 7

ER -