期刊
NATURE MEDICINE
卷 12, 期 11, 页码 1301-1309出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nm1492
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资金
- NIAID NIH HHS [R21 AI062718, T32 AI007244, AI09484, R01 AI045927-07, R01 AI009484, R01 AI009484-36, AI07244-22, AI062718-01, AI45927, R01 AI045927] Funding Source: Medline
- NINDS NIH HHS [NS048866-01, R21 NS048866] Funding Source: Medline
Persistent viral infections are a major health concern. One obstacle inhibiting the clearance of persistent infections is functional inactivation of antiviral T cells. Although such immunosuppression occurs rapidly after infection, the mechanisms that induce the loss of T-cell activity and promote viral persistence are unknown. Herein we document that persistent viral infection in mice results in a significant upregulation of interleukin (IL)-10 by antigen-presenting cells, leading to impaired T-cell responses. Genetic removal of II10 resulted in the maintenance of robust effector T-cell responses, the rapid elimination of virus and the development of antiviral memory T-cell responses. Therapeutic administration of an antibody that blocks the IL-10 receptor restored T-cell function and eliminated viral infection. Thus, we identify a single molecule that directly induces immunosuppression leading to viral persistence and demonstrate that a therapy to neutralize IL-10 results in T-cell recovery and the prevention of viral persistence.
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