Rock K L, Gramm C, Benacerraf B
Division of Lymphocyte Biology, Dana-Farber Cancer Institute, Boston, MA 02115.
Proc Natl Acad Sci U S A. 1991 May 15;88(10):4200-4. doi: 10.1073/pnas.88.10.4200.
RMA-S murine cells have a mutation that interferes with the assembly of class I major histocompatibility complex (MHC) heterodimers and are deficient in the expression of class I molecules on the cell surface. The mutant phenotype has been reported to be normalized upon incubation of RMA-S cells at 25 degrees C. We find that much of the increased expression of class I heterodimers is dependent on culturing RMA-S cells in bovine serum or with purified bovine beta 2-microglobulin. Furthermore, epitopes that are associated with class I MHC molecules that have bound xenogeneic beta 2-microglobulin are preferentially formed on RMA-S cells cultured at 25 degrees C. These heterologous class I molecules are thermolabile. Increased expression of class I molecules has also been observed on RMA-S cells incubated at 37 degrees C in the presence of class I-restricted peptides. We find that the increased expression of Db molecules induced by influenza virus nucleoprotein residues 365-380 is similarly dependent on culturing RMA-S cells in bovine serum or with purified bovine beta 2-microglobulin.
RMA - S小鼠细胞存在一种突变，该突变会干扰I类主要组织相容性复合体（MHC）异二聚体的组装，并且细胞表面I类分子的表达存在缺陷。据报道，将RMA - S细胞在25摄氏度下培养后，突变表型会恢复正常。我们发现，I类异二聚体表达的增加很大程度上依赖于在牛血清中培养RMA - S细胞或使用纯化的牛β2 - 微球蛋白培养。此外，与结合了异种β2 - 微球蛋白的I类MHC分子相关的表位，在25摄氏度下培养的RMA - S细胞上优先形成。这些异源I类分子是热不稳定的。在存在I类限制性肽的情况下，在37摄氏度下培养的RMA - S细胞上也观察到I类分子表达增加。我们发现，流感病毒核蛋白残基365 - 380诱导的Db分子表达增加同样依赖于在牛血清中培养RMA - S细胞或使用纯化的牛β2 - 微球蛋白培养。
