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|Title:||Lung endothelial cell antigen cross-presentation to CD8+T cells drives malaria-associated lung injury||Authors:||Claser, C.
Wu Howland, S.
Theng Theng Ho, J.
Bing Ong, C.
Guan Ng, L.
|Issue Date:||2019||Publisher:||Nature Publishing Group||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||Rights:||Attribution 4.0 International||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).||Source Title:||Nature Communications||URI:||https://scholarbank.nus.edu.sg/handle/10635/209515||ISSN:||2041-1723||DOI:||10.1038/s41467-019-12017-8||Rights:||Attribution 4.0 International|
|Appears in Collections:||Staff Publications|
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