Molecular mechanisms of and novel pathomorphological bases on vasculitis syndromes

血管细胞生物学的最新进展可能使阐明血管炎综合征的分子机制和病理形态基础成为可能。1)血管细胞表型表达的分子病理学分析：1)血管炎症中细胞和分子间的相互作用(黏附分子、组胺、一氧化氮、细胞凋亡、血管重塑)，2)血管生成(基因表达，成纤维细胞生长因子-2/血管内皮生长因子，一种新的内皮细胞分化途径，三维分析)，3)疾病特有的病理形态特征(IAAA，肺丛状血管病变，大动脉炎，MPA，胶原病肝内血管炎，动脉硬化，血管-血管炎)，2)血管损伤的影响和调节宿主因素：1)血管损伤的机制，动脉硬化，血管-血管炎血管炎的组织分布，肾小球病变的规律性变化，大动脉炎)，2)血清因子(抗内皮细胞抗体，大黄…更多的类母细胞因子、抗磷脂综合征、内皮细胞可吞噬的抗体)，3)T细胞克隆性(GCA，病理生理动力学，大动脉炎，动脉硬化)，4)溶酶体酶(川崎病)，3)血管炎的动物模型：1)川崎病(白念珠菌提取物诱导的小管炎，MPO基因敲除小鼠)，2)病毒依赖型血管炎(HTLV-1 env-PX转基因大鼠，HCMV-IE转基因小鼠)，3)MRL小鼠的胶原性脉管炎(受IRF-1反式基因和趋化因子拮抗剂基因转移的抑制)，4)基因组分析：1)Takayasu炎(人类白细胞抗原多态，HLA多态，基因敲除小鼠)，2)病毒依赖性小血管炎(HTLV-1 env-PX转基因大鼠，HCMV-IE转基因小鼠)，3)MRL小鼠的胶原性疾病(IRF-1反式基因和趋化因子拮抗剂的基因转移抑制)，4)基因组分析：1)Takayasu炎(人类白细胞抗原)4)川崎病模型小鼠(抗脉管炎基因)，5)5个校外研讨会：1)“2000年系统性脉管炎国际研讨会”，2)“2000年东京系统性脉管炎国际研讨会”，2)“脉管炎研究新进展”，松山，2002年2月16日。较少

Recent advances in vascular cell biology may make it possible to clarify the molecular mechanisms and pathomorphological bases of vasculitis syndromes. We thus performed several projects to take a new turn as follows.1 Molecular pathological analyses of the phenotypic expression of vascular cells: 1) cross talks among cells and molecules in vasculitis (adhesion molecules, histamine, NO, apoptosis, vascular remodeling), 2) angiogenesis (gene expression, FGF-2/VEGF, a new differentiation pathway of endothelial cells, three dimensional analysis), 3) pathomorphological features specific for diseases (IAAA, pulmonary plexiform angiopathy, Takayasu arteritis, MPA, intra-hepatic vasculitis in collagen disease, arteriosclerosis, vasa-vasoritis),2 Affecting and modifying host factors in vascular injury: 1) ANCA (mechanisms of vascular injury, tissue distribution of vasculitis, regular variations of glomerular lesions, Takayasu arteritis), 2) serum factors (anti-endothelial cell antibodies, rheu … More matoid factors, anti-phospholipid syndrome, antibodies phagocytizable by endothelial cells), 3) T cell clonalities (GCA, pathophysiological dymanics, Takayasu arteritis, arteriosclerosis), 4) lysosomal enzymes (Kawasaki disease),3 Animal models for vasculitis: 1) Kawasaki disease (C.albicans extract-induced vasculitis, MPO- knock out mice), 2) Virus-dependent vasculitis (HTLV-1 env-pX transgenic rat, HCMV-IE transgenic mice), 3) MRL mice for vasculitis in collagen disease (inhibition by IRF-1 trans gene and gene transfer of chemokine antagonist),4 Genome analysis: 1) Takayasu arteritis (HLA polymorphism, SNP of lKBL1), 2) geographical pathology (Takayasu arteritis), 3) MRL mouse vasculitis (positional candidate genes, blood vessel-caliber specific gene loci, 35 recombinat inbred strains for vasculitis research), 4) Kawasaki disease model mice (vasculitis-resistant loci),5 Extramural seminars: 1) "International Workshop on Systemic Vasculitis 2000", Tokyo, Oct. 14, 2000, 2) "New Developments in Vasculitis Research", Matsuyama, Feb. 16, 2002. Less