Nádasdy T, Kemény E, Krenács T, Csajbók E, Szenohradszky P, Stiller D, Ormos J
Pathológiai Inttezete, Szent-Györgyi Albert Orvostudományi Egyetem.
Morphol Igazsagugyi Orv Sz. 1990 Jul;30(3):208-19.
Authors examined cells participating in intimaproliferation in transplantation arteriopathy ultrastructurally in needle and wedge biopsy material from 40 transplanted kidneys, and immunohistochemically in 10 cases. In early biopsies--even in two control kidneys--it could be observed that the smooth muscle cells of media are in direct contact with endothel cells by their small processes. Processes can fulfil a receptor function and can transmit endothel noxa to smooth muscle cells. Smooth muscle cells of media react to endothel damage caused by rejection with migration to intima and during this period they are transformed to myofibroblasts (myointimal cells). In the mean time inflammatory cells (mainly macrophages, helper and cytotoxic cells in lower number) from the lumen infiltrate the intima, and mediators, enzymes released from them can inspire smooth muscle cells to further proliferation, migration to intima and transformation to myofibroblast. To effect of mediators (gamma interferon) released from inflammatory cells, the myointimal cells during rejection will press out 2nd class transplantation antigens (HLA-DR), and as vicious circle it further aggravates immune reply to graft, causing vascular damage, intimaproliferation.
作者对40例移植肾的针吸活检和楔形活检材料进行了超微结构检查，以观察参与移植性动脉病变内膜增殖的细胞，并对其中10例进行了免疫组织化学检查。在早期活检中——甚至在两个对照肾中——可以观察到，中膜的平滑肌细胞通过其小突起与内皮细胞直接接触。这些突起可以发挥受体功能，并将内皮损伤因素传递给平滑肌细胞。中膜的平滑肌细胞对排斥反应引起的内皮损伤作出反应，迁移至内膜，在此期间它们转变为肌成纤维细胞（肌内膜细胞）。与此同时，来自管腔的炎性细胞（主要是巨噬细胞，少量辅助性和细胞毒性细胞）浸润内膜，它们释放的介质和酶可促使平滑肌细胞进一步增殖、迁移至内膜并转变为肌成纤维细胞。在炎性细胞释放的介质（γ干扰素）作用下，排斥反应期间的肌内膜细胞会表达Ⅱ类移植抗原（HLA-DR），这会形成恶性循环，进一步加重对移植物的免疫反应，导致血管损伤和内膜增殖。
