共 40 条
Type I interferon induces CX3CL1 (fractalkine) and CCL5 (RANTES) production in human pulmonary vascular endothelial cells
被引:54
作者:

Nakano, M.
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机构:
Kyoto Univ, Dept Rheumatol & Clin Immunol, Grad Sch Med, Kyoto 6068507, Japan
Kyoto Univ, Dept Appl Lab Sci, Grad Sch Med, Kyoto 6068507, Japan Kyoto Univ, Dept Control Rheumat Dis, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan

Fujii, T.
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h-index: 0
机构:
Kyoto Univ, Dept Control Rheumat Dis, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan
Kyoto Univ, Dept Rheumatol & Clin Immunol, Grad Sch Med, Kyoto 6068507, Japan Kyoto Univ, Dept Control Rheumat Dis, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan

Hashimoto, M.
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机构: Kyoto Univ, Dept Control Rheumat Dis, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan

Yukawa, N.
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h-index: 0
机构:
Kyoto Univ, Dept Rheumatol & Clin Immunol, Grad Sch Med, Kyoto 6068507, Japan Kyoto Univ, Dept Control Rheumat Dis, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan

Yoshifuji, H.
论文数: 0 引用数: 0
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机构:
Kyoto Univ, Dept Rheumatol & Clin Immunol, Grad Sch Med, Kyoto 6068507, Japan Kyoto Univ, Dept Control Rheumat Dis, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan

Ohmura, K.
论文数: 0 引用数: 0
h-index: 0
机构:
Kyoto Univ, Dept Rheumatol & Clin Immunol, Grad Sch Med, Kyoto 6068507, Japan Kyoto Univ, Dept Control Rheumat Dis, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan

Nakaizumi, A.
论文数: 0 引用数: 0
h-index: 0
机构:
Kyoto Univ, Dept Appl Lab Sci, Grad Sch Med, Kyoto 6068507, Japan Kyoto Univ, Dept Control Rheumat Dis, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan

Mimori, T.
论文数: 0 引用数: 0
h-index: 0
机构:
Kyoto Univ, Dept Rheumatol & Clin Immunol, Grad Sch Med, Kyoto 6068507, Japan Kyoto Univ, Dept Control Rheumat Dis, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan
机构:
[1] Kyoto Univ, Dept Control Rheumat Dis, Grad Sch Med, Sakyo Ku, Kyoto 6068507, Japan
[2] Kyoto Univ, Dept Rheumatol & Clin Immunol, Grad Sch Med, Kyoto 6068507, Japan
[3] Kyoto Univ, Dept Appl Lab Sci, Grad Sch Med, Kyoto 6068507, Japan
关键词:
CCL5 (RANTES);
connective tissue disease;
CX3CL1 (fractalkine);
pulmonary vascular disease;
type I interferon;
SYSTEMIC-LUPUS-ERYTHEMATOSUS;
ARTERIAL-HYPERTENSION;
RHEUMATOID-ARTHRITIS;
MULTIPLE-SCLEROSIS;
CHEMOKINE;
EXPRESSION;
RECEPTOR;
BETA;
MANIFESTATIONS;
ACTIVATION;
D O I:
10.1111/j.1365-2249.2012.04638.x
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Type I interferon (IFN) medications cause various adverse reactions, including vascular diseases. Although an association between chemokines and vascular diseases has also been reported, the relationship between type I IFN and chemokines in vascular endothelial cells (VEC) remains unclear. To provide clues to pathogenesis of the diseases, we analysed the effects of type I IFN on chemokine production in human VEC. Type I IFN induced higher CX3CL1 (fractalkine) mRNA expression and protein secretion in pulmonary arterial VEC than in umbilical vein VEC. Type I IFN also induced CCL5 [regulated upon activation normal T cell expressed and secreted (RANTES)] production in VEC, especially in lung micro-VEC. IFN-beta induced much higher chemokine production than IFN-a, and Janus protein tyrosine kinase (JAK) inhibitor I prevented type I IFN-induced chemokine secretion. Type I IFN-induced chemokines may be involved in the pathophysiology of pulmonary vascular diseases, and the JAK inhibitor may serve as a therapeutic option for these diseases.
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页码:94 / 100
页数:7
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