SEROLOGICAL AND BIOCHEMICAL-ANALYSIS OF IA MOLECULES IN THE I-A MUTANT B6.C-H-2BM121

SEROLOGICAL AND BIOCHEMICAL-ANALYSIS OF IA MOLECULES IN THE I-A MUTANT B6.C-H-2BM121
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DOI:
10.1097/00007890-198106000-00006
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发表时间:
1981-01-01
期刊:
影响因子:
6.2
通讯作者:
DAVID, CS
DAVID, CS
中科院分区:
医学2区
文献类型:
--
作者:
LAFUSE, WP;MCCORMICK, JF;DAVID, CS

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菌株B6.C-H-2bm 12在小鼠H-2基因复合体的I-A亚区中具有突变,其引起皮肤移植排斥、混合淋巴细胞反应(MLR)和Ia抗原表达的改变。该突变影响正常脾细胞上Ia.3、8、9、15和20的表达。当脾细胞用脂多糖(LPS)刺激时,发现所有Ia特异性的表达,除了Ia.8 Ia分子,当用3 H-亮氨酸内部标记时,可以用针对a.3、9、15和20的抗血清沉淀,但不能用Ia.8沉淀。当突变bm 2和无关单倍型之间产生F1时,Ia.3、9、15和20可以通过对正常脾细胞的微量细胞毒试验检测到,但不能检测到Ia.8。该突变明显影响在正常脾细胞表面上表达的Ia分子的量,或者该分子不适当地锚定在细胞表面中,使得其不能用于细胞毒性和放射性碘化。特异性Ia.8,可能是一个组合决定子,显然在突变体中不存在,这是因为其中一条链的结构改变,可能是β链。链这种突变显然不涉及Ae链。这一发现相对于I区介导的同种异体识别和抗原呈递的意义进行了讨论。
Strain B6.C-H-2bm12 has a mutation in the I-A subregion of the mouse H-2 gene complex, which causes skin graft rejection, mixed lymphocyte reaction (MLR) and alterations in the expression of Ia antigens. The mutation affects the expression of Ia.3, 8, 9, 15 and 20 on normal spleen cells. When the spleen cells were stimulated with lipopolysaccharide (LPS), the expression of all Ia specificities were found except Ia.8 Ia molecules when internally labeled with 3H-leucine can be precipitated with antisera directed against, a.3, 9, 15 and 20, but not Ia.8. When F1 are made between the mutant bm2 and unrelated haplotypes, Ia.3, 9, 15, and 20 can be detected by microcytotoxic assay on normal spleen cells, but not Ia.8. The mutation evidently affects either the amount of Ia molecules expressed on normal spleen cell surfaces or the molecule is anchored improperly in the cell surface such that it is not accessible for cytotoxicity and radioiodination. Specificity Ia.8, which may be a combinatorial determinant, apparently is absent in the mutant because of a structural alteration in 1 of the chains, probably the .beta. chain. The mmutation evidently does not involve the Ae chain. The significance of this finding relative to I region-mediated allorecognition and antigen presentation is discussed.