Autoimmune chronic spontaneous urticaria: What we know and what we do not know
Autoimmune chronic spontaneous urticaria: What we know and what we do not know
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DOI：
10.1016/j.jaci.2016.08.050
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发表时间：
2017-06-01
影响因子：
14.2
通讯作者：
Maurer, Marcus
中科院分区：
文献类型：
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作者：
Kolkhir, Pavel;Church, Martin K.;Maurer, Marcus
慢性自发性荨麻疹（CSU）是一种肥大细胞驱动的皮肤病，其特征是短暂性风团、血管性水肿或两者复发超过6周。自身免疫被认为是CSU最常见的原因之一。I型和II型自身免疫（即，分别针对自身变应原的IgE和针对IgE或其受体的IgG自身抗体）与CSU的病因和发病机制有关。我们分析了相关文献，并评估了现有的证据，以支持的作用，I型和II型自身免疫性CSU的帮助下，希尔的因果关系的标准。对于这些标准中的每一个（即，关联强度、一致性、特异性、时间性、生物梯度、可解释性、连贯性、实验和类比），我们将证据的强度分类为“不足”、“低”、“中等”，“或“高”，然后将CSU患者中I型和II型自身免疫的因果关系级别从1级分配至（因果关系）至5级（不太可能有因果关系）。基于支持Hill标准的证据，CSU患者的I型自身免疫具有3级因果关系（建议存在因果关系），II型自身免疫具有2级因果关系（可能存在因果关系）。CSU的病理机制仍有许多方面需要解决，但越来越清楚的是，至少有2种不同的途径，I型和II型自身免疫，有助于这种复杂疾病的发病机制。
Chronic spontaneous urticaria (CSU) is a mast cell-driven skin disease characterized by the recurrence of transient wheals, angioedema, or both for more than 6 weeks. Autoimmunity is thought to be one of the most frequent causes of CSU. Type I and II autoimmunity (ie, IgE to autoallergens and IgG autoantibodies to IgE or its receptor, respectively) have been implicated in the etiology and pathogenesis of CSU. We analyzed the relevant literature and assessed the existing evidence in support of a role for type I and II autoimmunity inCSUwith the help of Hill's criteria of causality. For each of these criteria (ie, strength of association, consistency, specificity, temporality, biological gradient, plausibility, coherence, experiment, and analogy), we categorized the strength of evidence as "insufficient," "low," "moderate," or "high" and then assigned levels of causality for type I and II autoimmunity in patients with CSU from level 1 (causal relationship) to level 5 (causality not likely). Based on the evidence in support of Hill's criteria, type I autoimmunity in patients with CSU has level 3 causality (causal relationship suggested), and type II autoimmunity has level 2 causality (causal relationship likely). There are still many aspects of the pathologic mechanisms of CSU that need to be resolved, but it is becoming clear that there are at least 2 distinct pathways, type I and type II autoimmunity, that contribute to the pathogenesis of this complex disease.