Flood P M, Benoist C, Mathis D, Murphy D B
Proc Natl Acad Sci U S A. 1986 Nov;83(21):8308-12. doi: 10.1073/pnas.83.21.8308.
One of the more intriguing puzzles in immunology is the genetic basis for control of murine T-cell I-J determinants. Molecules bearing I-J determinants (I-J molecules) play a role in information trafficking among immunocompetent cells, probably serving as self-recognition molecules that channel regulatory factors to their appropriate target cells. Although it is clear that I-J polymorphism is influenced by the major histocompatibility complex (MHC), molecular genetic studies provide evidence that an MHC gene does not encode I-J molecules. A possible explanation for this paradox is that I-J molecules are a set of non-MHC-encoded T cell receptors that are directly or indirectly selected for by self-MHC products. One key to resolving the genetic and molecular basis for control of I-J determinants is the identification of the MHC gene(s) involved. Herein, data are presented which show that E alpha transgenic mice express an altered I-J phenotype, providing clear evidence that I region class II genes influence I-J polymorphism. Although further study is required to resolve how class II genes mediate this effect, this is a major piece to the I-J puzzle.
免疫学中一个更引人入胜的谜题是小鼠T细胞I-J决定簇控制的遗传基础。带有I-J决定簇的分子(I-J分子)在免疫活性细胞间的信息传递中发挥作用,可能作为自我识别分子,将调节因子导向其合适的靶细胞。虽然很明显I-J多态性受主要组织相容性复合体(MHC)影响,但分子遗传学研究提供的证据表明,一个MHC基因并不编码I-J分子。对于这一矛盾的一个可能解释是,I-J分子是一组非MHC编码的T细胞受体,它们被自身MHC产物直接或间接选择。解决I-J决定簇控制的遗传和分子基础的一个关键是鉴定相关的MHC基因。在此展示的数据表明,Eα转基因小鼠表达改变的I-J表型,这为I区II类基因影响I-J多态性提供了明确证据。虽然需要进一步研究来解决II类基因如何介导这种效应,但这是I-J谜题的一个主要部分。