1. Autoimmune chronic spontaneous urticaria: What we know and what we do not know 
Pavel Kolkhir, MD, Martin K. Church, PhD, DSc, Karsten Weller, MD, Martin Metz, MD, Oliver Schmetzer, MD, Marcus Maurer, MD 
Journal of Allergy and Clinical Immunology 
Volume 139, Issue 6, Pages e1 (June 2017)
DOI: /j.jaci
Copyright © 2016 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2. Fig 1
Mechanisms of mast cell activation in patients with chronic spontaneous autoimmune urticaria. Type I autoimmunity: Type I autoantigens (“autoallergens”) can activate mast cells and basophils by crosslinking IgE-AAbs. Type II autoimmunity: IgG-AAbs can do the same by binding to IgE or to FcεRI, which might involve complement C5a and the CD88/C5aR receptor. IgG-AAbs against the low-affinity IgE receptor (FcεRII) might activate eosinophils and induce subsequent mast cell degranulation. ECP, Eosinophil cationic protein; LTs, leukotrienes; MBP, major basic protein; PAF, platelet-activating factor; SCF, stem cell factor; VEGF, vascular endothelial growth factor.
Journal of Allergy and Clinical Immunology  , e1DOI: ( /j.jaci )
Copyright © 2016 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3. Fig 2
Possible actions of omalizumab in patients with CSU with type I or II autoimmunity. Type I autoimmunity (rapid response to treatment): In patients with type I autoimmune (“autoallergic”) CSU, omalizumab neutralizes IgE-AAbs and forms omalizumab-IgE immune complexes that might bind type I autoantigens (“autoallergens”). Type II autoimmunity (slower response to treatment): Downregulation of free IgE results in downregulation of FcεRI expression on mast cells, which reduces their activation by IgG–anti-IgE and IgG–anti-FcεRI.
Journal of Allergy and Clinical Immunology  , e1DOI: ( /j.jaci )
Copyright © 2016 American Academy of Allergy, Asthma & Immunology Terms and Conditions