| Peripheral nerve injuries are very commonly seen in the clinic. If they cannot be immediately repaired to recover continuity and integrity, they often result in motor and sensory deficits for patients. In many instances these injuries result in long nerve segment loss preventing the nerve ends from being directly sutured due to increased tension. In these cases grafts such as autografts and allografts must be used to bridge the long nerve gaps. Although autografts are recognized as the gold standard for nerve grafting, they have several limitations including limited donor source, functional loss in the distribution of the donor nerve, scarring, and painful neuroma formation. Allografts also have defects in limitations of source. In order to find a means of reconstructing injured nerves, peripheral nerve xenotransplantation has become an increasingly promising alternative.Compared with heart, renal and other organs transplantation, peripheral nerve xenografts are just as the tube for nerve regeneration and play the role at the primary period. If the injuried nerve have regenerated and controlled the muscle, whether the xenografts exist will not be important for recipients. The cytokines secreted by thl cells are recognized as the major factors, and can promote the transplant rejection induced by the specific CTL and TDTH. Th2cells can inhibit the function of Th1. Th1/Th2paradigm is the center of the rejection mechanism and has been accepted by researchers. Recent studies demonstrate that Thl7and IL-17take part in the rejection of renal, heart, lung and liver transplantation. During peripheral nerve xenotransplantation, what is the regulatory mechanism between Thl and Thl7; what kind of cells plays the major role; whether the rejection can be prevented by blocking the role of these two kinds of cells? I performed the peripheral nerve xenotransplantation from rats to mouse, and get the conclusion:1Compared with peripheral nerve autotransplantation, mononuclear cells invasion increased during peripheral never xenotransplantation acute rejection; IFN-γ+,IL-17+cells invasion also increased around the surrounding tissues of xenografts; the levels of IFN-γ,IL-17increased in serum; the expression of IFN-γ,IL-17in lymphocytes from spleen increased. The changes of IL-4had no significant differences.2After using IFN-y neutralizing antibodies, although there is no significant difference of IFN-γ,IL-17expression in serum and lymphocytes from spleen compared to the xenografts recipients without injecting neutralizing antibodies, IFN-γ+,IL-17+cells invasion decreased around the surrounding tissues of xenografts.3After using IL-17neutralizing antibodies,IFN-γ,IL-17decreased in serum, spleen and surrounding tissues of xenografts.4The results in xenografts recipients of IFN-γ and IL-17neutralizing antibodies mixed used were similar as the recipients with IL-17neutralizing antibodies single used.5IFN-γ and IL-17play the crucial role during the acute rejection of peripheral nerve xenotransplantation; Thl7can play the role respectively, and are not dependent Thl; the rejection of peripheral nerve xenotransplantation by blocking the function of IFN-γ and IL-17.This study is the primary research about the role of Thl/Thl7during acute rejection of peripheral nerve xenotranspantation, and about the mechanism of rejection after using IFN-γ and IL-17neutralizing antibodies. The conclusion can provide the data and method for preventing the rejection and clinical treatment. Although Thl and Thl7play the role during the rejection, the regulatory mechanism between these two kinds of cells and the relationship between innate and adaptive immune cells need to be further studied. I hope do my best for clinical use of peripheral nerve xeontransplantation. |
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