Moyer C F, Jerome W G, Taylor R, Tulli H, Reinisch C L
Department of Comparative Medicine, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, North Carolina.
Autoimmunity. 1992;12(3):159-65. doi: 10.3109/08916939209148455.
The pathogenesis of autoimmune vasculitis is poorly understood. Understanding the immunologic mechanisms governing this disease requires precise identification of the cells which comprise the lesion. In this report, we have evaluated tissue sections from MRL/lpr mice from 16 to 45 weeks of age, representing all stages of clinical vasculitis. We demonstrate that basophil myelocytes participate in the evolution of the delayed-type hypersensitivity (DTH) response which initiates and perpetuates autoimmune vasculitis in these mice. These findings raise questions regarding the immunologic mechanisms by which basophils develop in this lesion and the interaction of basophils. VSMCs and lymphocytes in vasculitic angiodestruction.
自身免疫性血管炎的发病机制尚不清楚。要了解控制这种疾病的免疫机制,需要精确识别构成病变的细胞。在本报告中,我们评估了16至45周龄MRL/lpr小鼠的组织切片,这些小鼠代表了临床血管炎的所有阶段。我们证明嗜碱性粒细胞髓细胞参与了迟发型超敏反应(DTH)的演变,该反应启动并维持了这些小鼠的自身免疫性血管炎。这些发现引发了关于嗜碱性粒细胞在该病变中发育的免疫机制以及嗜碱性粒细胞、血管平滑肌细胞(VSMCs)和淋巴细胞在血管炎性血管破坏中的相互作用的问题。