作者: George Tellides , Denis A. Tereb , Nancy C. Kirkiles-Smith , Richard W. Kim , Jean H. Wilson
DOI: 10.1038/35003221
关键词: Transplantation 、 Arteriosclerosis 、 Interferon gamma 、 Antigen presentation 、 Vascular smooth muscle 、 Immunology 、 Atheroma 、 Cancer research 、 Biology 、 Cytokine 、 Signal transduction
摘要: Atherosclerosis and post-transplant graft arteriosclerosis are both characterized by expansion of the arterial intima as a result infiltration mononuclear leukocytes, proliferation vascular smooth muscle cells (VSMCs) accumulation extracellular matrix. They also associated with presence immunomodulatory cytokine interferon-gamma (IFN-gamma). Moreover, in mouse models atheroma formation or allogeneic transplantation, serological neutralization genetic absence IFN-gamma markedly reduces extent intimal expansion. However, other studies have found that exogenous inhibits cultured VSMC matrix synthesis, response to mechanical injury. This discrepancy is generally explained idea either directly activates macrophages, or, increasing antigen presentation, indirectly T within lesions atherosclerosis arteriosclerosis. These activated leukocytes thought express VSMC-activating cytokines cell-surface molecules cause observed arteriosclerotic responses. Here we inserted pig human arteries into aorta immunodeficient mice, show can induce changes detectable immunocytes acting on VSMCs potentiate growth-factor-induced mitogenesis.