van Vliet E, Molenaar J L, Tuk C W, Bruining G J, de Vries R R
Tissue Antigens. 1987 Apr;29(4):195-200. doi: 10.1111/j.1399-0039.1987.tb01576.x.
Aberrant expression of major histocompatibility (MHC) antigens has been implicated as a factor contributing to organ-specific autoimmunity, such as progressive loss of pancreatic beta cells in type 1 diabetes. We investigated the potential of a rat beta cell tumour, RINM5F, to express enhanced levels of MHC antigens in vitro. To this purpose we treated RINM5F cells in vitro with recombinant rat gamma interferon (rIF gamma). We used monoclonal antibodies to RT1.A (class I) and RT1.B (class II) antigens of the rat MHC in conjunction with flowcytometry and immunoperoxidase techniques to analyse the expression of MHC antigens. Untreated RINM5F cells express low levels of RT1.A, whereas they are negative for RT1.B. Treatment with rIF gamma appeared to increase the expression of RT1.A antigens substantially. Most importantly, RT1.B antigens were newly expressed by rat insulinoma cells in vitro after treatment with rIF gamma. To our knowledge this is the first documentation of the potential of beta cells or their derivatives to express class II MHC antigens following IF gamma-treatment. This mechanism may play an important role in the augmentation and perpetuation of insulitis leading to type 1 diabetes mellitus.
主要组织相容性（MHC）抗原的异常表达被认为是导致器官特异性自身免疫的一个因素，例如1型糖尿病中胰腺β细胞的逐渐丧失。我们研究了大鼠β细胞瘤RINM5F在体外表达增强水平MHC抗原的潜力。为此，我们在体外用重组大鼠γ干扰素（rIFγ）处理RINM5F细胞。我们使用针对大鼠MHC的RT1.A（I类）和RT1.B（II类）抗原的单克隆抗体，结合流式细胞术和免疫过氧化物酶技术来分析MHC抗原的表达。未经处理的RINM5F细胞表达低水平的RT1.A，而它们对RT1.B呈阴性。用rIFγ处理似乎显著增加了RT1.A抗原的表达。最重要的是，用rIFγ处理后，大鼠胰岛素瘤细胞在体外新表达了RT1.B抗原。据我们所知，这是首次记录β细胞或其衍生物在IFγ处理后表达II类MHC抗原的潜力。这种机制可能在导致1型糖尿病的胰岛炎的加剧和持续中起重要作用。
