Murine marrow coexpressing H2-Dsp2 and H2-Db on host natural killer cell rejection.
Murine marrow coexpressing H2-Dsp2 and H2-Db on host natural killer cell rejection.
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小鼠骨髓共表达 H2-Dsp2 和 H2-Db 对宿主自然杀伤细胞排斥。
DOI：
10.1097/00007890-199702150-00019
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发表时间：
1997
期刊：
影响因子：
6.2
通讯作者：
Bennett,M
中科院分区：
文献类型：
--
作者：
Liu,J;Sentman,CL;Kumar,V;Bennett,M
背景：I 类分子可能抑制或激活自然杀伤 (NK) 细胞。骨髓细胞 (BMC) 上的 H2-D d、-L d 或 -D sp2（后者源自 spretus 小鼠）会被 NK1 识别和排斥。 1+ NK 细胞。分析了 H2 sp2 和 H2 b 之间的 H2 内重组体的 BMC。 9347 和 R40 K b I b Bat2 b/Tnf sp2 D sp2 BMC 被 B6 主机拒绝。然而，B6 主机分别拒绝和接受 K b D sp2 D b R40× B6 和 9347× B6 BMC。因此，D b 和/或H2-Bat2/Tnf间隔基因可以调节H2-D sp2+ BMC的免疫原性。方法。R40或9347小鼠与DBA杂交。 D b (H2 d, D b)转基因小鼠产生F1和F2后代。宿主脾脏中的DNA合成（增殖）是骨髓移植成功的衡量标准。结果。（1）H2 9347或R40+ H2 d-D b+（但不是D b-）F2后代的BMC在B6宿主中生长。（2）H2 9347或R40× DBA的BMC。 D b F1 K b/d D sp2/d D b 后代被 B6 排斥，但不被 B6D2F1 (H2 b/d) 或 D8 (H2 b, D d) 宿主排斥。(3) NK 细胞是效应细胞。结论。D b 可以降低 D sp2+ BMC (F2 数据) 的免疫原性，但不能降低 D d+ BMC (F1 数据) 的免疫原性。 F2 H2 R40 D b+（而非 F1 R40× B6）、BMC 移植物在 B6 宿主中的生长可能基于 H2-Bat2/Tnf 区域中的基因差异。或者，DBA/2 的非 H2 基因也可能参与其中。这些基因将为 D b 重链提供肽，形成“保护基序”，向宿主 NK 细胞发送负信号。
Background.Class I molecules may inhibit or activate natural killer (NK) cells. H2-D d,-L d, or-D sp2 (the latter derived from spretus mice) on bone marrow cells (BMC) are recognized and rejected by NK1. 1+ NK cells. BMC of intra-H2 recombinants between H2 sp2 and H2 b were analyzed. The 9347 and R40 K b I b Bat2 b/Tnf sp2 D sp2 BMC were rejected by B6 hosts. However, B6 hosts reject and accept K b D sp2 D b R40× B6 and 9347× B6 BMC, respectively. Thus, D b and/or H2-Bat2/Tnf interval genes may regulate the immunogenicity of H2-D sp2+ BMC.Methods.R40 or 9347 mice were crossed with DBA. D b (H2 d, D b) transgenic mice to produce F1 and F2 progeny. DNA synthesis (proliferation) in host spleens was the measure of marrow graft success.Results.(1) BMC of H2 9347orR40+ H2 d-D b+(but not D b-) F2 progeny grew in B6 hosts.(2) BMC of H2 9347orR40× DBA. D b F1 K b/d D sp2/d D b progeny were rejected by B6, but not by B6D2F1 (H2 b/d) or D8 (H2 b, D d) hosts.(3) NK cells were the effectors.Conclusions.D b can reduce the immunogenicity of D sp2+ BMC (F2 data), but not of D d+ BMC (F1 data). Growth of F2 H2 R40 D b+, but not F1 R40× B6, BMC grafts in B6 hosts could be based on gene (s) differences in the H2-Bat2/Tnf region. Alternatively, non-H2 genes of DBA/2 might be involved. The genes would provide peptides for D b heavy chains to form “protective motifs” that send negative signals to host NK cells.