The role of stress protein-reactive gammadeltaT cells in infection

我们已经报道了在李斯特菌感染的早期，对应激蛋白有反应的γ - eltat细胞增加。我们还发现应激蛋白反应性γ - eltat细胞在同基因混合淋巴细胞反应（MLR）中增加。从观察结果来看，我们估计细菌感染后自我应激蛋白/细菌应激蛋白交叉反应性γ - eltat细胞增加。因此，我们分析了自反应性γ - eltat细胞，以进一步了解应激蛋白反应性γ - eltat细胞的特性。我们建立了8个自反应性γ - γ细胞杂交瘤。4个杂交瘤表达Vdelta5, 4个杂交瘤表达Vdelta6。抗应激蛋白(Hsp60) -单克隆抗体ML30阻断了8个自反应性γ - γ细胞杂交瘤中7个的应答。由于不同T细胞受体的γ - eltat细胞杂交瘤的应答被ML30抗体阻断，我们推断Hsp60分子参与了γ - eltat细胞杂交瘤的抗原识别，而不是Hsp60的ML30表位。

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.