Please use this identifier to cite or link to this item:
https://doi.org/10.1038/s41467-019-12017-8
DC Field | Value | |
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dc.title | Lung endothelial cell antigen cross-presentation to CD8+T cells drives malaria-associated lung injury | |
dc.contributor.author | Claser, C. | |
dc.contributor.author | Nguee, S.Y.T. | |
dc.contributor.author | Balachander, A. | |
dc.contributor.author | Wu Howland, S. | |
dc.contributor.author | Becht, E. | |
dc.contributor.author | Gunasegaran, B. | |
dc.contributor.author | Hartimath, S.V. | |
dc.contributor.author | Lee, A.W.Q. | |
dc.contributor.author | Theng Theng Ho, J. | |
dc.contributor.author | Bing Ong, C. | |
dc.contributor.author | Newell, E.W. | |
dc.contributor.author | Goggi, J. | |
dc.contributor.author | Guan Ng, L. | |
dc.contributor.author | Renia, L. | |
dc.date.accessioned | 2021-12-06T04:20:11Z | |
dc.date.available | 2021-12-06T04:20:11Z | |
dc.date.issued | 2019 | |
dc.identifier.citation | Claser, C., Nguee, S.Y.T., Balachander, A., Wu Howland, S., Becht, E., Gunasegaran, B., Hartimath, S.V., Lee, A.W.Q., Theng Theng Ho, J., Bing Ong, C., Newell, E.W., Goggi, J., Guan Ng, L., Renia, L. (2019). Lung endothelial cell antigen cross-presentation to CD8+T cells drives malaria-associated lung injury. Nature Communications 10 (1) : 4241. ScholarBank@NUS Repository. https://doi.org/10.1038/s41467-019-12017-8 | |
dc.identifier.issn | 2041-1723 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/209515 | |
dc.description.abstract | Malaria-associated acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are life-threatening manifestations of severe malaria infections. The pathogenic mechanisms that lead to respiratory complications, such as vascular leakage, remain unclear. Here, we confirm that depleting CD8+T cells with anti-CD8? antibodies in C57BL/6 mice infected with P. berghei ANKA (PbA) prevent pulmonary vascular leakage. When we transfer activated parasite-specific CD8+T cells into PbA-infected TCR??/? mice (devoid of all T-cell populations), pulmonary vascular leakage recapitulates. Additionally, we demonstrate that PbA-infected erythrocyte accumulation leads to lung endothelial cell cross-presentation of parasite antigen to CD8+T cells in an IFN??dependent manner. In conclusion, pulmonary vascular damage in ALI is a consequence of IFN?-activated lung endothelial cells capturing, processing, and cross-presenting malaria parasite antigen to specific CD8+T cells induced during infection. The mechanistic understanding of the immunopathogenesis in malaria-associated ARDS and ALI provide the basis for development of adjunct treatments. © 2019, The Author(s). | |
dc.publisher | Nature Publishing Group | |
dc.rights | Attribution 4.0 International | |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0/ | |
dc.source | Scopus OA2019 | |
dc.type | Article | |
dc.contributor.department | MICROBIOLOGY AND IMMUNOLOGY | |
dc.description.doi | 10.1038/s41467-019-12017-8 | |
dc.description.sourcetitle | Nature Communications | |
dc.description.volume | 10 | |
dc.description.issue | 1 | |
dc.description.page | 4241 | |
Appears in Collections: | Staff Publications Elements |
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