期刊
CELL
卷 162, 期 5, 页码 1078-1089出版社
CELL PRESS
DOI: 10.1016/j.cell.2015.08.021
关键词
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资金
- NIH/NCI Cancer Center Support Grant (CCSG) [P30CA008748]
- NIH [R37AI034206]
- Ludwig Center at Memorial Sloan Kettering Cancer Center
- Hilton-Ludwig Cancer Prevention Initiative (Conrad N. Hilton Foundation)
- Hilton-Ludwig Cancer Prevention Initiative (Ludwig Cancer Research)
- Robert Black Fellowship of the Damon Runyon Cancer Research Foundation [DRG-2143-13]
- Irvington Fellowship of the Cancer Research Institute
Regulatory T (Treg) cells suppress immune responses to a broad range of non-microbial and microbial antigens and indirectly limit immune inflammation-inflicted tissue damage by employing multiple mechanisms of suppression. Here, we demonstrate that selective Treg cell deficiency in amphiregulin leads to severe acute lung damage and decreased blood oxygen concentration during influenza virus infection without any measureable alterations in Treg cell suppressor function, antiviral immune responses, or viral load. This tissue repair modality is mobilized in Treg cells in response to inflammatory mediator IL-18 or alarmin IL-33, but not by TCR signaling that is required for suppressor function. These results suggest that, during infectious lung injury, Treg cells have a major direct and non-redundant role in tissue repair and maintenance-distinct from their role in suppression of immune responses and inflammation-and that these two essential Treg cell functions are invoked by separable cues.
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