Chung D H, Dorfman J, Plaksin D, Natarajan K, Belyakov I M, Hunziker R, Berzofsky J A, Yokoyama W M, Mage M G, Margulies D H
Molecular Biology and Lymphocyte Biology Sections, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA.
J Immunol. 1999 Oct 1;163(7):3699-708.
We generated transgenic mice expressing a single-chain beta2-microglobulin (beta2m)-H-2Dd. The cell-surface beta2m-H-2Dd molecule was expressed on a beta2m-deficient background and reacted with appropriate mAbs. It was of the expected m.w. and directed the normal development of CD8+ T cells in the thymus of a broad TCR repertoire. It also presented both exogenously provided and endogenous peptide Ags to effector CD8+ T cells. In tests of NK cell education and function, it failed to reveal any interaction with NK cells, suggesting that the site of the interaction of NK receptors with H-2Dd was disrupted. Thus, the sites of TCR and NK receptor interaction with H-2Dd are distinct, an observation consistent with independent modes of TCR and NK receptor evolution and function.
我们培育出了表达单链β2-微球蛋白(β2m)-H-2Dd的转基因小鼠。细胞表面的β2m-H-2Dd分子在β2m缺陷背景下表达,并与合适的单克隆抗体发生反应。它具有预期的分子量,并指导了广泛TCR库的胸腺中CD8+T细胞的正常发育。它还将外源性提供的和内源性的肽抗原呈递给效应CD8+T细胞。在自然杀伤(NK)细胞的教育和功能测试中,它未能揭示与NK细胞的任何相互作用,这表明NK受体与H-2Dd的相互作用位点被破坏。因此,TCR和NK受体与H-2Dd的相互作用位点是不同的,这一观察结果与TCR和NK受体进化及功能的独立模式一致。