한빛사논문
In-Ho Seo1,5, Hyuk Soo Eun2,5, Ja Kyung Kim3,5, Hoyoung Lee1, Seongju Jeong1, Seong Jin Choi1, Jeewon Lee1, Byung Seok Lee2, Seok Hyun Kim2, Woo Sun Rou2, Dong Hyeon Lee4, Won Kim4,*, Su-Hyung Park1,*, Eui-Cheol Shin1,5,6,*
1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 34141, Republic of Korea
2Department of Internal Medicine, Chungnam National University School of Medicine, Daejeon 35015, Republic of Korea
3Department of Internal Medicine, Yongin Severance Hospital, Yonsei University College of Medicine, Yongin 16995, Republic of Korea
4Department of Internal Medicine, Seoul Metropolitan Government Seoul National University Boramae Medical Center, Seoul National University College of Medicine, Seoul 07061, Republic of Korea
5These authors contributed equally
6Lead contact
*Corresponding author
Abstract
During microbial infection, bystander CD8+ T cells that are not specific to infecting pathogens can be activated by interleukin (IL)-15. However, the tissue-homing properties of bystander-activated CD8+ T cells have not been elucidated. Here, we examine the effects of IL-15 on the expression of chemokine receptors on CD8+ T cells and their migration. IL-15 upregulates CCR5 in memory CD8+ T cells in the absence of T cell receptor (TCR) stimulation and enhances CCR5-dependent migration. IL-15-induced CCR5 upregulation is abrogated by TCR stimulation, indicating that CCR5 is upregulated in bystander-activated CD8+ T cells. Moreover, CCR5 signals increase proliferation and cytotoxic protein expression in IL-15-treated memory CD8+ T cells, although the increase has a small extent. CCR5 upregulation in bystander-activated CD8+ T cells is associated with severe liver injury in patients with acute hepatitis A. Altogether, the results indicate that CCR5 upregulation by IL-15 mediates the migration of bystander-activated CD8+ T cells.
Keywords : IL-15, bystander-activated CD8+ T cells, CCR5, migration
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