Journal
CELL REPORTS
Volume 36, Issue 4, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2021.109438
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Funding
- Samsung Science and Technology Foundation [SSTF-BA1402-51]
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IL-15 upregulates CCR5 in memory CD8(+) T cells, enhancing their migration, while the upregulation is abrogated by TCR stimulation. CCR5 signals increase proliferation and cytotoxic protein expression in IL-15-treated memory CD8(+) T cells, associating with severe liver injury in patients with acute hepatitis A.
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.
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