REJECTION OF CLASS-I MHC-DEFICIENT HEMATOPOIETIC-CELLS BY IRRADIATED MHC-MATCHED MICE
REJECTION OF CLASS-I MHC-DEFICIENT HEMATOPOIETIC-CELLS BY IRRADIATED MHC-MATCHED MICE
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DOI：
10.1038/349329a0
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发表时间：
1991-01-24
期刊：
影响因子：
64.8
通讯作者：
RAULET, D
中科院分区：
文献类型：
--
作者：
BIX, M;LIAO, NS;RAULET, D
照射的MHC-杂合小鼠经常排斥从纯合亲本品系之一移植的骨髓细胞，这种现象（“杂交抗性”）似乎违反了移植定律1，2。 亲本和同种异体骨髓细胞的排斥也不同于常规T细胞介导的排斥机制，因为它受NK 1.1+细胞3-5的影响。 为了解释骨髓排斥的不寻常特异性，已经提出NK 1.1+细胞破坏不能表达自身MHC I类（MHC-I）分子的完整补体的骨髓细胞5。 我们在这里表明，正常小鼠中的NK 1.1+细胞排斥来自缺乏正常细胞表面MHC-I表达的小鼠的造血移植物，这是因为β 2-微球蛋白基因6-9中的靶向突变。 这些发现表明，MHC-I分子的表达缺陷使骨髓细胞对排斥反应敏感。
IRRADIATED MHC-heterozygous mice often reject bone marrow cells transplanted from one of the homozygous parental strains, a phenomenon ('hybrid resistance') that appears to violate the laws of transplantation 1,2. Rejection of parental and allogeneic marrow cells also differs from conventional T cell-mediated rejection mechanisms as it is effected by NK1.1+ cells 3-5. To account for the unusual specificity of bone marrow rejection, it has been proposed that NK1.1+ cells destroy marrow cells that fail to express the full complement of self MHC class I (MHC-I) molecules 5. We show here that NK1.1+ cells in normal mice reject haemopoietic transplants from mice that are deficient for normal cell-surface MHC-I expression because of a targeted mutation in the beta-2-microglobulin gene 6-9. These findings demonstrate that deficient expression of MHC-I molecules renders marrow cells susceptible to rejection.