Molina Vered, Shoenfeld Yehuda
Department of Medicine B and The Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel.
Autoimmunity. 2005 May;38(3):235-45. doi: 10.1080/08916930500050277.
The etiology of autoimmune diseases is still not clear but genetic, immunological, hormonal and environmental factors are considered to be important triggers. Most often autoimmunity is not followed by clinical symptoms unless an additional event such as an environmental factor favors an overt expression. Many environmental factors are known to affect the immune system and may play a role as triggers of the autoimmune mosaic.Infections: bacterial, viral and parasitic infections are known to induce and exacerbate autoimmune diseases, mainly by the mechanism of molecular mimicry. This was studied for some syndromes as for the association between SLE and EBV infection, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection and more. Vaccines, in several reports were found to be temporally followed by a new onset of autoimmune diseases. The same mechanisms that act in infectious invasion of the host, apply equally to the host response to vaccination. It has been accepted for diphtheria and tetanus toxoid, polio and measles vaccines and GBS. Also this theory has been accepted for MMR vaccination and development of autoimmune thrombocytopenia, MS has been associated with HBV vaccination. Occupational and other chemical exposures are considered as triggers for autoimmunity. A debate still exists about the role of silicone implants in induction of scleroderma like disease.Not only foreign chemicals and agents have been associated with induction of autoimmunity, but also an intrinsic hormonal exposure, such as estrogens. This might explain the sexual dimorphism in autoimmunity.Better understanding of these environmental risk factors will likely lead to explanation of the mechanisms of onset and progression of autoimmune diseases and may lead to effective preventive involvement in specific high-risk groups. So by diagnosing a new patient with autoimmune disease a wide anamnesis work should be done.
自身免疫性疾病的病因仍不明确，但遗传、免疫、激素和环境因素被认为是重要的触发因素。大多数情况下，自身免疫并不伴有临床症状，除非诸如环境因素等额外事件有利于显性表达。已知许多环境因素会影响免疫系统，并可能作为自身免疫拼图的触发因素发挥作用。感染：细菌、病毒和寄生虫感染已知可诱发和加重自身免疫性疾病，主要通过分子模拟机制。针对一些综合征进行了研究，如系统性红斑狼疮与EB病毒感染之间的关联、与链球菌感染相关的儿童自身免疫性神经精神疾病等。在几份报告中发现，接种疫苗后会在一段时间后出现新的自身免疫性疾病发作。宿主对感染的免疫反应机制同样适用于宿主对疫苗接种的反应。对白喉和破伤风类毒素、脊髓灰质炎和麻疹疫苗以及格林-巴利综合征（GBS）而言，这一观点已被接受。这一理论也适用于麻疹、腮腺炎、风疹（MMR）疫苗接种与自身免疫性血小板减少症的发生，多发性硬化症与乙肝疫苗接种有关。职业和其他化学暴露被认为是自身免疫的触发因素。关于硅胶植入物在诱发硬皮病样疾病中的作用仍存在争议。不仅外来化学物质和制剂与自身免疫的诱发有关，内在的激素暴露，如雌激素，也与之有关。这可能解释了自身免疫中的性别差异。更好地了解这些环境风险因素可能会解释自身免疫性疾病的发病和进展机制，并可能导致对特定高危人群进行有效的预防性干预。因此，对于诊断为自身免疫性疾病的新患者，应进行全面的病史询问。
