The role of stress protein-reactive gammadeltaT cells in infection

我们已经报道，在李斯特林感染的早期阶段，对应激蛋白有反应的GammadeltaT细胞增加。我们还发现，在同基因混合淋巴细胞反应(MLR)中，应激蛋白反应性伽马德兰T细胞增加。通过观察，我们估计在细菌感染后，自身应激蛋白/细菌应激蛋白-交叉反应性伽马德兰T细胞增加。因此，我们对自身反应性的GammadeltaT细胞进行了分析，以进一步了解应激蛋白反应性的GammadeltaT细胞的特征。4株杂交瘤表达Vdelta5，4株杂交瘤表达Vdelta6。抗应激蛋白(HSP60)-单抗ML30阻断了8个具有自身反应性的γ-T细胞杂交瘤的反应。由于具有不同T细胞受体的T细胞杂交瘤的反应被ML30抗体阻断，我们推测HSP60分子而不是HSP60的ML30表位参与了T细胞杂交瘤的抗原识别。

We have reported that gammadeltaT cells reactive to stress protein increase at early stage of Listeriainfection. We also found that stress protein-reactive gammadeltaT cells increase in syngeneic mixed lymphocyte reaction (MLR). From the observations, we estimated that self stress protein/bacterial stress protein-cross reactive gammadeltaT cells increase after bacterial infection. Therefore we analyzed self-reactive gammadeltaT cells to know further characteristics of stress protein-reactive gammadeltaT cells.We establisher 8 self-reactive gammadeltaT cell hybridomas. Four hybridomas expressed Vdelta5 and four hybridomas expressed Vdelta6. Response of seven out of eight self-reactive gammadeltaT cell hybridomas was blocked by anti stress protein (Hsp60) -monoclonal antibody ML30. Since response of gammadeltaT cell hybridomas with different T cell receptor was blocked with the ML30 antibody, we reasoned that Hsp60 molecule, but not ML30 epitope of Hsp60, participate in antigen recognition by the gammadeltaT cell hybridomas.