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IMMUNOBIOLOGY OF THE HEMOPOIETIC HISTOCOMPATIBILITY

造血组织相容性的免疫生物学

基本信息

批准号：
3181778
负责人：
ICHIRO NAKAMURA
金额：
$ 12.98万
依托单位：
STATE UNIVERSITY OF NEW YORK AT BUFFALO
依托单位国家：
美国
项目类别：
财政年份：
1986
资助国家：
美国
起止时间：
1986-08-01 至 1990-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/3181778
关键词：
bone marrow transplantation gel electrophoresis gene expression genetic regulation genetic transcription graft versus host disease heterozygote histocompatibility gene homologous transplantation hybrid cells immunity laboratory mouse major histocompatibility complex neoplasm /cancer transplantation radioimmunoassay surface antigens transfection

项目摘要

The objective of this proposal is to dissect the little known mechanism(s), underlying murine natural resistance to normal and malignant hemopoietic cells, which paradoxically manifests itself in F1 hybrid recipients of parental grafts (hybrid resistance) and is mediated by natural killer (NK) cell-like effectors. The expression of the putative target cell surface structure and its recognition by the effectors, are immunogenetically specific and controlled by a class of seemingly "noncodominant" genes of limited polymorphism, i.e., the Hh (for hemopoietic histocompatibility) genes. It is the primary purpose of the proposed study to apply the techniques of molecular genetics to understand the genetic basis of hybrid resistance controlled by one of the Hh loci, the Hh-1, that maps to the H-2D region of the 17th chromosome. Two alternative hypotheses that may explain the "noncodominance" will be tested primarily by DNA-mediated gene transfer; a cis-acting mechanism of noncodominant expression would be supported if a Hh-1- phenotype is converted to a Hh-1+ phenotype by transfecting a Hh-1- cell with DNA from Hh-1+ strain of mouse, whereas a trans-acting genetic mechanism of noncodominance would be implicated if Hh-1 expression is suppressed by transfer of a DNA molecule from a Hh-1- strain into a Hh-1+ cell. With this approach, the H-2D region gene encoding or regulating the expression of Hh-1-controlled structures can be identified and isolated. Ultimately, the nature of these cell surface target structures, their expression and function in normal and abnormal (leukemic) hemopoiesis, and a physiological role of Nk-like cells recognizing such structures, may be defined. This study, therefore, should help unravel an important, possibly regulatory, function of the major histocompatibility complex and true functions of a class of lymphoid cells, i.e., the NK cells.

本提案的目的是剖析鲜为人知的机制，潜在的小鼠对正常和恶性造血细胞的天然抗性细胞，这矛盾地表现在F1杂交受体，亲本移植物（杂交抗性）并由自然杀伤细胞（NK）介导细胞样效应物。假定的靶细胞表面的表达结构及其识别的效应，是免疫遗传学特定的，并由一类看似“非共显性”的基因控制，有限的多态性，即，Hh（造血组织相容性）基因. 拟议研究的主要目的是应用分子遗传学技术，以了解杂种的遗传基础由Hh基因座之一Hh-1控制的抗性，该基因座映射到 17号染色体的H-2D区域。两种可能的假设解释“非共显性”将主要通过DNA介导的基因进行测试转移;非共显性表达的顺式作用机制将是如果Hh-1-表型通过以下方式转化为Hh-1+表型，则支持用来自Hh-1+小鼠品系的DNA转染Hh-1-细胞，而用来自Hh-1+小鼠品系的DNA转染Hh-1-细胞。如果存在非共显性的反式作用遗传机制， Hh-1表达通过从Hh-1 - 1细胞转移DNA分子而被抑制。菌株进入Hh-1+细胞。通过这种方法，H-2D区域基因编码或调节Hh-1控制的结构的表达，识别和隔离。最终，这些细胞表面的性质靶结构，它们在正常和异常中的表达和功能（白血病）造血和NK样细胞的生理作用识别这些结构，可以被定义。因此，这项研究应有助于解开一个重要的，可能是监管，功能的主要组织相容性复合体和一类淋巴样细胞的真正功能，也就是说，NK细胞。

项目成果

期刊论文数量（4）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Hemopoietic histocompatibility (Hh-1) phenotype and the regulation of its expression.

造血组织相容性（Hh-1）表型及其表达的调节。

DOI：
10.1007/bf00189521
发表时间：
1992
期刊：
Immunogenetics
影响因子：
3.2
作者：
Kaminsky,SG;Yoshida,MA;Milisauskas,VK;Nakamura,I
通讯作者：
Nakamura,I

The B144-H-2Db interval and the location of a mouse homologue of the human D6S81E locus.

B144-H-2Db 间隔和人类 D6S81E 基因座的小鼠同源物的位置。

DOI：
10.1007/bf02114974
发表时间：
1990
期刊：
Immunogenetics
影响因子：
3.2
作者：
Wroblewski,JM;Kaminsky,SG;Milisauskas,VK;Pittman,AM;Chaplin,DD;Spies,T;Nakamura,I
通讯作者：
Nakamura,I

Acute rejection of allogeneic hemopoietic progenitors by genetically resistant mice.

遗传抗性小鼠对同种异体造血祖细胞的急性排斥。