Minoda M, Senda S, Horiuchi A
J Clin Lab Immunol. 1987 Jun;23(2):101-8.
Whether a defect the syngeneic mixed lymphocyte reaction (SMLR) is caused by an abnormality in the recognition of autoantigen (Ia antigen) by T cells or by an abnormality in macrophages (Mø) which provides the Ia antigen was examined using New Zealand black (NZB) mice, a model animal for human autoimmune diseases. The level of activation of T cells by Ia antigen was lower in NZB mice than in normal mice, despite the fact that the quantity of Ia antigen expressed on the surface of Mø was much the same in the NZB mice. Furthermore, less Ia antigen was expressed on thymic reticuloepithelial cells (TRC) in NZB mice than in normal mice. These findings suggest that the defect in the SMLR in NZB mice is mainly due to T cells, namely, to abnormality in the activation of the Ia antigen receptors on the T cells, which occurs as a result of the contact between T cells and TRC in the process of T cell maturation and differentiation.
利用人类自身免疫性疾病的模型动物新西兰黑(NZB)小鼠,研究了同基因混合淋巴细胞反应(SMLR)缺陷是由T细胞识别自身抗原(Ia抗原)异常引起,还是由提供Ia抗原的巨噬细胞(Mø)异常所致。尽管NZB小鼠Mø表面表达的Ia抗原量与正常小鼠大致相同,但NZB小鼠中Ia抗原对T细胞的激活水平低于正常小鼠。此外,NZB小鼠胸腺网状上皮细胞(TRC)上表达的Ia抗原比正常小鼠少。这些发现表明,NZB小鼠SMLR缺陷主要归因于T细胞,即T细胞成熟和分化过程中T细胞与TRC接触导致T细胞上Ia抗原受体激活异常。