Journal
JOURNAL OF IMMUNOLOGY
Volume 194, Issue 12, Pages 5801-5811Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1401936
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Funding
- Basic Science Research Program [2013R1A1A2010389]
- Bio and Medical Technology Development Program of the National Research Foundation of Korea - Ministry of Education [2012M3A9B4028264]
- Ministry of Science, ICT and Future Planning
- Korean Health Technology R&D Project through the Korea Health Industry Development Institute - Ministry of Health and Welfare [HI13C0833]
- Yonsei University Research Fund
- POSCO TJ Park Foundation, Republic of Korea
- Korea Health Promotion Institute [0920040, 0920040-1] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [2012H1A2A1016220] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Regulatory T (T-reg) cells act as terminators of T cell immuniy during acute phase of viral infection; however, their role and suppressive mechanism in chronic viral infection are not completely understood. In this study, we compared the phenotype and function of T-reg cells during acute or chronic infection with lymphocytic choriomeningitis virus. Chronic infection, unlike acute infection, led to a large expansion of T-reg cells and their upregulation of programmed death-1 (PD-1). T-reg cells from chronically infected mice (chronic T-reg cells) displayed greater suppressive capacity for inhibiting both CD8(+) and CD4(+) T cell proliferation and subsequent cytokine production than those from naive or acutely infected mice. A contact between T-reg and CD8(+) T cells was necessary for the potent suppression of CD8(+) T cell immune response. More importantly, the suppression required cell-specific expression and interaction of PD-1 on chronic T-reg cells and PD-1 ligand on CD8(+) T cells. Our study defines PD-1 upregulated on T-reg cells and its interaction with PD-1 ligand on effector T cells as one cause for the potent T cell suppression and proposes the role of PD-1 on T-reg cells, in addition to that on exhausted T cells, during chronic viral infection.
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