弥漫性淋巴结微血管病变是长期胰岛素依赖糖尿病患者免疫缺陷的并发原因

P. Muretto
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摘要

在体外模型中已经证实了遗传性(1型)自身免疫性(2型)和代谢性(1型和2型)胰岛素依赖型糖尿病(IDDM)的免疫异常。然而,糖尿病患者对频繁和持久感染易感性增加的确切原因尚不清楚,尽管大量体外研究集中在免疫细胞的代谢和功能改变上。糖尿病微血管病变是一种特殊的疾病改变,已在视网膜、肾小球、皮肤、骨骼肌、周围神经和其他器官中广泛描述,但未在淋巴结中描述。我们报告了4例长期IDDM、严重淋巴细胞减少症和多种传染性疾病患者尸检过程中多处切除淋巴结的组织学和免疫组织化学观察结果。这种特殊的微血管病变改变是由透明物质的存在引起的,薄血管和毛细血管的基底膜增厚,与淋巴结B细胞和T细胞依赖区域的淋巴耗损以及滤泡树突状网状细胞(FDRC)的显著减少同时发生。事实上,微血管病变进一步损害T淋巴细胞和B淋巴细胞的运输和渗出,可能会阻止内皮细胞向FDRC的转化,并导致淋巴滤泡严重的免疫功能衰竭。本研究的组织学和免疫组织化学数据可以为糖尿病患者免疫缺陷的复杂问题提供额外的见解。
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Diffuse Lymph-Nodes Microangiopathy as Concurrent Cause of Immunodeficiency in Long-Term Insulin-Dependent Diabetic Patients
Immune abnormalities have been demonstrated in vitro models in genetic (type1) autoimmune (type 2) and metabolic (type 1 and type 2) Insulin-Dependent Diabetes Mellitus (IDDM). However, the precise reason for increased susceptibility to frequent and protracted infections in diabetic patients is still unclear, despite a multitude of in vitro studies which have focused on the metabolic and functional modifications of immune cells Diabetes microangiopathy, which is a peculiar alteration of the disease, has been extensively described in the retina, renal glomeruli, skin, skeletal muscles, peripheral nerves, and other organs but not in lymph nodes. We report our histological and immunohistochemical observations in lymph-nodes removed in multiple sites during autopsy from four patients with long-term IDDM, severe lymphocytpenia and several infectious diseases during their life. The peculiar microangiopathic modifications made by presence of hyaline substance thickening basal membrane of thin vessels and capillaries appear concurrent with lymphodepletion of B and T cells dependent areas of lymph-nodes and with jointed marked reduction of Follicular Dendritic Reticulum Cells (FDRC). Indeed microangiopathy further compromise the traffic and diapedesis of T and B lymphocytes may prevent the transformation of endothelial cells into FDRC with severe immune failure of lymphoid follicles. The histological and immunohistochemical data in this study could provide additional insights into the complex problem of the immunodeficiency in diabetic patients.
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