| Background information:Transplanting gradually becomes the primary Rx to cure some terminal kidney, liver, heart and lung diseases. The long-term using of immunosuppressor (as ciclosporin A,FK506) not only spends too much but also always leads to serious side effects, such as occasional infections, arteriosclerosis, damage to the liver and kidney and malignancy as well. So what needs our primal concern is that we should find an effective way to let the body accept the transplanted organ without the using of immunosuppressor. The kernel of transplant repulsion is T cells chain immune response which is mainly caused by TCR recognizing the homogeneous but hetero-type antigen on the surface of transplanted organ. During this course, APC (antigen presenting cell) is of crucial importance. DC (dendritic cell) is the body's full-time APC. It can not only activate the resting T cells through antigen and costimulatory molecules, bringing about differentiation of the T cells, clone expansion and immune responsion, but also by means of apoptosis, inability and growth of the adjusting T cells. Experiments proves that MHC I, II and costimulatory molecules B7-1 (CD80), B7-2 (CD86), CD40 can hardly be observed in the immature DC. So the DC induces the inability or apoptosis of T cells while it shows antigen. This is called the veto effect which shows its unique application value in transplant immunity. However, when the immature DC enters the body, the MHC II and B7-2 molecules will be increased and become mature. So, we must find a new way to let DC remain immature at certain times when injected into the body and restrain the acute repulsion or induce endurance to the maximum extent. Research proves that TGF-β1 is a kind of modulating gene which can immunosuppress and restrain transplant repulsion. The gene modification project provides...
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