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在bm13突变体中未检测到三个Db区域控制分子(H-2D1b、H-2D2b、H-2Lb)中的一个(H-2D2b)。

One (H-2D2b) of the three Db region-controlled molecules (H-2D1b, H-2D2b, H-2Lb) is not detected in bm13 mutant.

作者信息

Iványi D, Démant P

出版信息

J Immunol. 1983 Sep;131(3):1080-4.

PMID:6604086
Abstract

Analysis of the antigenic heterogeneity of Db region products by the technique of antibody-induced redistribution of cell surface antigens (capping) revealed the existence of two types of H-2 molecules reactive with the monoclonal anti-Db antibody, B22-249R 1 (H-2.m2). The relationship of the two H-2.2-positive molecules described here is similar to that of H-2D and H-2M detected in the products of the Dd region; they differ in the repertoire of the H-2 public specificities, although they share the private specificity. We designate them, in accordance to recently proposed nomenclature, H-2D1b and H-2D2b. Both types of molecule have been detected on T lymphocytes of C57BL/6 (H-2b), C3H.B10(H-2b), and B10.A(2R) (H-2h2, KkDb) strains. In mutant strain B6.C-H-2bm13, however, only one type of H-2.2-positive molecule, H-2D1b, could be detected. This finding resembles the situation in the d haplotype, in which mutant strain B10.D2 (M504) (H-2dm1) had only one molecule (H-2Dd), of the two H-2.4-positive molecules H-2Dd and H-2Md that could be detected. A third Db region molecule, H-2Lb, does not carry the Db private specificity H-2.2, and it is detectable by some of the antibodies against the H-2.28 family of specificities; it is distinct from the Qa-2 molecule. The H-2Lb molecule was detected in all strains tested in this experiment, including the bm13 mutant.

摘要

通过抗体诱导细胞表面抗原重分布(封帽)技术分析Db区域产物的抗原异质性,发现存在两种与单克隆抗-Db抗体B22-249R 1(H-2.m2)反应的H-2分子。此处描述的两种H-2.2阳性分子的关系类似于在Dd区域产物中检测到的H-2D和H-2M的关系;它们在H-2公共特异性的库中有所不同,尽管它们共享私有特异性。根据最近提出的命名法,我们将它们命名为H-2D1b和H-2D2b。在C57BL/6(H-2b)、C3H.B10(H-2b)和B10.A(2R)(H-2h2,KkDb)品系的T淋巴细胞上均检测到了这两种分子。然而,在突变品系B6.C-H-2bm13中,只能检测到一种H-2.2阳性分子,即H-2D1b。这一发现类似于d单倍型中的情况,在d单倍型中,突变品系B10.D2(M504)(H-2dm1)在可检测到的两种H-2.4阳性分子H-2Dd和H-2Md中只有一种分子(H-2Dd)。第三个Db区域分子H-2Lb不携带Db私有特异性H-2.2,并且可以被一些针对H-2.28特异性家族的抗体检测到;它与Qa-2分子不同。在本实验测试的所有品系中均检测到了H-2Lb分子,包括bm13突变体。

相似文献

1
One (H-2D2b) of the three Db region-controlled molecules (H-2D1b, H-2D2b, H-2Lb) is not detected in bm13 mutant.在bm13突变体中未检测到三个Db区域控制分子(H-2D1b、H-2D2b、H-2Lb)中的一个(H-2D2b)。
J Immunol. 1983 Sep;131(3):1080-4.
2
Characterization of H-2Db antigens implies haplotype differences in the number of H-2 molecules expressed.H-2Db抗原的特征表明,在表达的H-2分子数量上存在单倍型差异。
J Immunol. 1982 Jul;129(1):222-6.
3
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J Immunol. 1983 Nov;131(5):2440-4.
4
Recognition of H-2Kb mutant target cells by Moloney virus-specific cytotoxic T lymphocytes from bm13 (H-2Db mutant) mice. I. Full recognition of Kbm11 by Kb-restricted CTL.来自bm13(H-2Db突变体)小鼠的莫洛尼病毒特异性细胞毒性T淋巴细胞对H-2Kb突变靶细胞的识别。I. Kb限制性细胞毒性T淋巴细胞对Kbm11的完全识别。
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Private specificity of H-2Ldx molecule detected serologically by a surface antigen redistribution method (capping).通过表面抗原再分布法(帽化)血清学检测到的H-2Ldx分子的独特特异性。
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J Immunol. 1982 Feb;128(2):807-10.

引用本文的文献

1
Primary structural evidence that the H-2Dq region encodes at least three distinct gene products: Dq, Lq, and Rq.H-2Dq区域编码至少三种不同基因产物(Dq、Lq和Rq)的主要结构证据。
Proc Natl Acad Sci U S A. 1984 Apr;81(8):2499-503. doi: 10.1073/pnas.81.8.2499.
2
A monomorphic HLA-specific monoclonal antibody, W6/32, reacts with the H-2Db molecule of normal mouse lymphocytes.一种单克隆HLA特异性单克隆抗体W6/32与正常小鼠淋巴细胞的H-2Db分子发生反应。
Immunogenetics. 1984;20(6):699-703. doi: 10.1007/BF00430328.
3
Serological and immunochemical analysis of H-2 class I molecules encoded by the Db region.
对由Db区域编码的H-2 I类分子进行血清学和免疫化学分析。
Immunogenetics. 1984;20(3):341-5. doi: 10.1007/BF00364215.
4
A molecular hybrid of the H-2Dd and H-2Ld genes expressed in the dm1 mutant.在dm1突变体中表达的H-2Dd和H-2Ld基因的分子杂种。
Proc Natl Acad Sci U S A. 1984 Aug;81(16):5204-8. doi: 10.1073/pnas.81.16.5204.
5
Monoclonal antibody characterization of a unique immune response control locus between H-2S and D.H-2S与D之间独特免疫反应控制位点的单克隆抗体特性分析
J Exp Med. 1985 Nov 1;162(5):1477-93. doi: 10.1084/jem.162.5.1477.
6
Class I genes and molecules: an update.I类基因与分子:最新进展
Immunology. 1986 Jan;57(1):3-18.