Autoimmune chronic spontaneous urticaria: what we know and what we don’t know

Publication date: Available online 21 October 2016
Source:Journal of Allergy and Clinical Immunology
Author(s): Pavel Kolkhir, Martin K. Church, Karsten Weller, Martin Metz, Oliver Schmetzer, Marcus Maurer
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 type II autoimmunity, i.e. 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 in CSU with the help of Hill's criteria of causality. For each of these criteria, i.e. 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 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 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 two distinct pathways, type I and type II autoimmunity, that contribute to the pathogenesis of this complex disease.



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