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[Stimulation of T-lymphocytes by autologous monocytes. Decrease in the proliferative response in Gougerot-Sjögren
A mixed autologous culture enables the measurement of the proliferative response of T lymphocytes which have been stimulated by preparations of autologous mononucleated cells. The role of the monocytes present in the preparation was examined in this study which sought to determine if the autologous response induced by these monocytes was modified during Sjögren's syndrome. Purified monocytes are a powerful stimulant of autologous response in normal subjects. However, high concentrations of monocytes were found to have an inhibiting effect. In patients with Sjögren syndrome, the autologous response induced by monocytes in significantly decreased. This decrease parallels a reduction on "non-T" lymphocytes observed in these same patients. The anomaly provoking these two modifications does not appear to be caused by a seric factor or by a deficit of the proliferation of responding T lymphocytes. It is more likely due to a blockage of lymphocyte T/monocyte interactions where the markers of the HLA-D system intervene.
A mixed autologous culture enables the measurement of the proliferative response of T lymphocytes which have been stimulated by preparations of autologous mononucleated cells. The role of the monocytes present in the preparation was examined in this study which sought to determine if the autologous response induced by these monocytes was modified during Sjögren's syndrome. Purified monocytes are a powerful stimulant of autologous response in normal subjects. However, high concentrations of monocytes were found to have an inhibiting effect. In patients with Sjögren syndrome, the autologous response induced by monocytes in significantly decreased. This decrease parallels a reduction on "non-T" lymphocytes observed in these same patients. The anomaly provoking these two modifications does not appear to be caused by a seric factor or by a deficit of the proliferation of responding T lymphocytes. It is more likely due to a blockage of lymphocyte T/monocyte interactions where the markers of the HLA-D system intervene.