Autoimmune diseases and autoimmunity post-bone marrow transplantation
Autoimmune diseases and autoimmunity post-bone marrow transplantation
复制标题
DOI：
10.1038/sj.bmt.1701437
复制
发表时间：
1998-11-01
影响因子：
4.8
通讯作者：
Shoenfeld, Y
中科院分区：
文献类型：
--
作者：
Sherer, Y;Shoenfeld, Y
骨髓移植既能传播又能消除自身免疫性疾病，因此被认为是严重自身免疫性疾病的一种可选治疗方法。在这篇文章中，我们讨论了慢性GVHD本身是否是一种自身免疫性疾病的问题，回顾了人类BR IT后自身免疫性疾病的文献报道，并描述了BMT后状态的自身免疫性。慢性移植物抗宿主病是骨髓移植后常见的并发症，其临床和致病特征与硬皮病、干燥综合征等自身免疫性疾病相似。虽然慢性GVHD的发病机制尚不清楚，但急性GVHD引起的胸腺损伤可能与慢性GVHD的免疫缺陷和自身免疫有关。类似的现象是同基因GVHD，其由自身反应性和自身调节性淋巴细胞之间的失衡引起。此外，在BMT后患者中已经报道了其他自身免疫性疾病，并且其中最常见的是甲状腺功能减退症、甲状腺功能亢进症、重症肌无力和免疫性血细胞减少症。虽然这些疾病也发生在BMT后环境之外，但它们在发病机制（重症肌无力和胸腺病理学之间没有关联）、诊断（甲状腺功能亢进症的症状可能无意中与其他疾病相关）和预后（BMT后自身免疫性血细胞减少症可能是致命的，治疗无反应）方面是独特的。然而，许多其他自身免疫性疾病已报告后BMT，这些主要是作为病例报告。关于骨髓移植后自身免疫的机制，少数病例源于供体相关的致病性淋巴细胞或其祖细胞的转移，而大多数病例（慢性GVHD或特定疾病）可归因于骨髓移植后的免疫失衡。可能使个体暴露于BMT后自身免疫发展的因素包括遗传易感性、环境因素如CMV和可能有助于产生微嵌合体和随后的慢性GVHD及其相关自身免疫表现的供体的性质。
BMT can both transmit and eliminate autoimmune diseases, and hence it has been suggested as an optional treatment for severe autoimmune conditions. In this communication we deal with the question of whether chronic GVHD is an autoimmune disease in itself, review the literature reports of autoimmune diseases following BR IT in humans, and describe the autoimmune nature of the post-BMT state. Chronic GVHD, which is a frequent complication post-BMT, has clinical and pathogenic characteristics similar to autoimmune diseases, such as scleroderma and Sjogren's syndrome. Although the pathogenesis of chronic GVHD is not yet clear, thymic damage induced by acute GVHD may contribute to both the immunodeficiency and autoimmunity characterising chronic GVHD. A similar phenomenon is syngeneic GVHD, which results from an imbalance between autoreactive and autoregulatory lymphocytes, Additionally, other autoimmune diseases have been reported in post-BMT patients, and among these the most common are hypothyroidism, hyperthyroidism, myasthenia gravis and immune cytopenias. Although these diseases also occur also outside the post-BMT setting, they are unique with respect to pathogenesis (no association between myasthenia gravis and thymic pathology), diagnosis (symptoms of hyperthyroidism may be inadvertently related to other conditions), and prognosis (post-BMT autoimmune cytopenias may be fatal and treatment non-responsive). Nevertheless, many other autoimmune diseases have been reported after BMT, and these are mainly presented as case reports. Regarding the mechanism of post-BMT autoimmunity, the minority of cases stem from donor-related transfer of pathogenic lymphocytes or their progenitors, while most of the cases (either chronic GVHD or specific diseases) can be attributed to the immunologic imbalances characterising the post-BMT setting. The factors that may expose an individual to autoimmunity development post-BMT include genetic predisposition, an environmental factor such as CMV, and the nature of the donor who may aid in creating microchimerism and subsequently chronic GVHD and its related autoimmune manifestations.