Upregulation of SR-PSOX/CXCL16 and Recruitment of CD8 + T Cells in Cardiac Valves During Inflammatory Valvular Heart Disease-Reference-Cited by-同舟云学术

Upregulation of SR-PSOX/CXCL16 and Recruitment of CD8 + T Cells in Cardiac Valves During Inflammatory Valvular Heart Disease

Published:2004-02 Issue:2 Volume:24 Page:282-287
ISSN:1079-5642
Container-title:Arteriosclerosis, Thrombosis, and Vascular Biology
language:en
Short-container-title:ATVB

Author:

Yamauchi Ryoko¹,Tanaka Makoto¹,Kume Noriaki¹,Minami Manabu¹,Kawamoto Takahiro¹,Togi Kiyonori¹,Shimaoka Takeshi¹,Takahashi Shu¹,Yamaguchi Junko¹,Nishina Takeshi¹,Kitaichi Masanori¹,Komeda Masashi¹,Manabe Toshiaki¹,Yonehara Shin¹,Kita Toru¹

Affiliation:

1. From the Department of Cardiovascular Medicine (R.Y., N.K., T.K.), Graduate School of Medicine, Kyoto University, Kyoto, Japan; the Department of Social Service (M.T.), Kyoto University Hospital, Kyoto, Japan; the Department of Geriatric Medicine (M.T., M.M., T.K., K.T.), Graduate School of Medicine, Kyoto University, Kyoto, Japan; the Institute for Viral Research (T.S., S.Y.), Kyoto University, Kyoto, Japan; Biomedical Research Laboratories (S.T., J.Y.), Sankyo Co., Ltd, Tokyo, Japan; the...

Abstract

Objective— SR-PSOX/CXCL16 is a transmembrane chemokine and is implicated in activated CD8 + T cell trafficking. In the present study, we examined the expression pattern of SR-PSOX/CXCL16 in the heart and investigated a potential role of SR-PSOX/CXCL16 in inflammatory valvular heart disease. Methods and Results— Initial expression of SR-PSOX/CXCL16 in murine embryos was detected in endothelial cells lining endocardial cushions in the forming heart at E11.5. From mid-gestation to adult, expression of this gene in the heart was exclusively observed in valvular endothelial cells. Examination of SR-PSOX/CXCL16 expression in human cardiac valves demonstrated that SR-PSOX/CXCL16 was strongly expressed in valvular and neocapillary endothelial cells in patients with infective endocarditis. SR-PSOX/CXCL16 expression in neocapillary endothelial cells was also observed in patients with rheumatic and atherosclerotic valvular disease. Moreover, CD8 + T cells were distributed closely to endothelial cells expressing SR-PSOX/CXCL16. In vitro adhesion assays showed that SR-PSOX/CXCL16 induced adhesion of activated CD8 + T cells to vascular cell adhesion molecule-1 (VCAM-1) through very late antigen-4 (VLA-4) activation. Furthermore, SR-PSOX/CXCL16 stimulated interferon-γ (IFN-γ) production by CD8 + T cells. Conclusions— SR-PSOX/CXCL16 may be involved in CD8 + T cell recruitment through VLA-4 activation and stimulation of IFN-γ production by CD8 + T cells during inflammatory valvular heart disease.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

Link

https://www.ahajournals.org/doi/pdf/10.1161/01.ATV.0000114565.42679.c6

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