期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 39, 期 10, 页码 2800-2808出版社
WILEY-V C H VERLAG GMBH
DOI: 10.1002/eji.200939508
关键词
CD30; Cytomegalovirus; NK cells
类别
资金
- Wellcome Trust
- Medical Research Council [G9818340B] Funding Source: researchfish
The pathogenic outcomes of viral infection are often reminiscent of a dysfunctional immune system. Thus, cytomegalovirus (CMV) causes disruption of the lymphoid architecture and the functionality of lymphocytes, both of which are features of CD30 deficiency. It was therefore plausible that CD30 might interfere with CMV infection. The present study identifies CD30 as an inducible NK-cell receptor critical for innate immunity against CMV. Expression of CD30 integrates survival signals to NK cells that allow them to prevent viral spread and subsequent disintegration of secondary lymphoid tissue. Deficiency in CD30 results in exaggerated NK cell death and complete abrogation of the lymphoid architecture. Our data define the necessity of NK cells for protection of secondary lymphoid organs and describe a mechanism by which this protection is conferred.
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