Journal
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
Volume 170, Issue 1, Pages 94-100Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1365-2249.2012.04638.x
Keywords
CCL5 (RANTES); connective tissue disease; CX3CL1 (fractalkine); pulmonary vascular disease; type I interferon
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Funding
- Japanese Ministry of Education, Culture, Sports, Science and Technology
- Japanese Ministry of Health, Labor and Welfare
- Smoking Research Foundation
- Grants-in-Aid for Scientific Research [22390201, 22591091] Funding Source: KAKEN
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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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