期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 198, 期 8, 页码 1213-1224出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20030918
关键词
thymocyte development; bone marrow chimera; NK cell toxicity; CD8 T cells; retroviral infection
资金
- NIAID NIH HHS [R01 AI033456, R01 AI33456] Funding Source: Medline
Natural killer cells gauge the absence of self class I MHC on susceptible target cells by means of inhibitory receptors such as members of the Ly49 family. To initiate killing by natural killer cells, a lack of inhibitory signals must be accompanied by the presence of activating ligands on the target cell. Although natural killer cell-mediated rejection of class I MHC-deficient bone marrow (BM) grafts is a matter of record, little is known about the targeting in vivo of specific cellular subsets by natural killer cells. We show here that development of class I MHC-negative thymocytes is delayed as a result of natural killer cell toxicity after grafting of a class I MHC-positive host with class I MHC-negative BM. Double positive thymocytes that persist in the presence of natural killer cells display an unusual T cell receptor deficient phenotype, yet nevertheless give rise to single positive thymocytes and yield mature class I MHC-deficient lymphocytes that accumulate in the class I MHC-positive host. The resulting class I MHC-deficient CD8 T cells are functional and upon activation remain susceptible to natural killer cell toxicity in vivo. Reconstitution of class I MHC-deficient BM precursors with H2-K-b by retroviral transduction fully restores normal thymic development.
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