Mac1阳性巨噬细胞的耗竭可保护DBA/2小鼠免受脑心肌炎病毒诱导的心肌炎和糖尿病的侵害。
Depletion of Mac1-positive macrophages protects DBA/2 mice from encephalomyocarditis virus-induced myocarditis and diabetes.
作者信息
Hirasawa K, Tsutsui S, Takeda M, Mizutani M, Itagaki S, Doi K
机构信息
Department of Biomedical Science, Faculty of Agriculture, University of Tokyo, Japan.
出版信息
J Gen Virol. 1996 Apr;77 ( Pt 4):737-41. doi: 10.1099/0022-1317-77-4-737.
DBA/2 mice treated with anti-Mac1 monoclonal antibody (MAb) failed to develop encephalomyocarditis virus (EMCV)-induced diabetes and myocarditis. Virus concentrations and the number of viral RNA-positive cells in the pancreas and heart were significantly reduced in mice treated with anti-Mac1 MAb. Mac1-positive macrophages seem to be involved in EMCV-induced disease and to affect the replication of EMCV in target organs.
用抗Mac1单克隆抗体（MAb）处理的DBA/2小鼠未能发生脑心肌炎病毒（EMCV）诱导的糖尿病和心肌炎。在用抗Mac1 MAb处理的小鼠中，胰腺和心脏中的病毒浓度以及病毒RNA阳性细胞数量显著降低。Mac1阳性巨噬细胞似乎参与了EMCV诱导的疾病，并影响EMCV在靶器官中的复制。
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