TRANSFER OF DIABETES IN MICE PREVENTED BY BLOCKADE OF ADHESION-PROMOTING RECEPTOR ON MACROPHAGES
TRANSFER OF DIABETES IN MICE PREVENTED BY BLOCKADE OF ADHESION-PROMOTING RECEPTOR ON MACROPHAGES
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DOI：
10.1038/348639a0
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发表时间：
1990-12-13
期刊：
影响因子：
64.8
通讯作者：
COOKE, A
中科院分区：
文献类型：
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作者：
HUTCHINGS, P;ROSEN, H;COOKE, A
胰岛素依赖型糖尿病（IDDM）是一种具有自身免疫病因的疾病。非肥胖糖尿病小鼠是人类疾病的良好自发动物模型，50-80% 的雌性小鼠在 6 个月大时会出现 IDDM1,2。该疾病可通过糖尿病供体的脾 T 细胞转移，并可通过 T 细胞耗竭来预防 3,4。 β 细胞被特异性破坏的机制尚不清楚，但基于浸润胰岛中巨噬细胞的存在以及慢性二氧化硅治疗预防疾病的能力，T 细胞和巨噬细胞都受到牵连5,6。单克隆抗体 5C6 对骨髓单核细胞粘附促进 3 型补体受体（CR3 或 CD11b/CD18）7 具有特异性，并且不与 T 细胞结合。在这里，我们证明体内巨噬细胞 CR3 的阻断可防止巨噬细胞和 T 细胞的胰岛内浸润，并抑制 IDDM 的发展。我们得出的结论是，T 细胞和巨噬细胞在 IDDM 的发病中发挥着重要作用。
INSULIN-dependent diabetes mellitus (IDDM) is a disease with an autoimmune aetiology. The non-obese diabetic mouse is a good spontaneous animal model of the human disease, with IDDM developing in 50–80% of female mice by the age of 6 months1,2. The disease can be transferred by splenic T cells from diabetic donors and is prevented by T-cell depletion3,4. The mechanism(s) by which the β cell is specifically destroyed is not known, but T cells and macrophages have both been implicated, based on the presence of macrophages in the infiltrated islet and the ability of chronic silica treatment to prevent disease5,6. The monoclonal antibody 5C6 is specific for the myelomonocytic adhesion-promoting type-3 complement receptor (CR3 or CD11b/CD18)7and does not bind to T cells. Here we show that blockade of macrophage CR3in vivoprevents intra-islet infiltration by both macrophages and T cells and inhibits development of IDDM. We conclude that both T cells and macrophages have an essential role in the onset of IDDM.