Autoreactive IgE in Chronic Spontaneous/Idiopathic Urticaria and Basophil/Mastocyte Priming Phenomenon, as a Feature of Autoimmune Nature of the Syndrome

Abstract

Recent years of research have shed a new light on the role of IgE in immune reactions. It seems to be more than just a contribution to immediate type of allergic response. It appears that monomeric IgE may enhance mast cell activity without cross-linking of FcεRI by IgE specific allergen or autoreactive IgG anti-IgE antibodies. Monomeric IgE molecules are heterogeneous concerning their ability to induce survival and activation of mast cells only by binding the IgE to FcεRI, but not affecting degranulation of cells. It also turned out that IgE may react to autoantigens occurring in the blood not only in chronic spontaneous urticaria (CSU) but also in other autoimmune diseases. The aforementioned phenomena may promote the activity of mast cells/basophils in CSU that easily degranulate when influenced by various inner (autoreactive IgG against IgE and FcεRI, autoreactive IgE for self-antigens) and outer factors (cold, heat, pressure) or allergens. These findings forced the new approach to the role of autoimmunity, self-antigens and IgE autoantibodies in the pathology of CSU. CSU put in the scheme of autoreactive IgG and autoreactive IgE seems to be either a kind of an autoimmune disease or a clinical manifestation of some other defined autoimmune diseases or both.

The overlap syndrome of urticaria and gastroesophageal reflux disease

“…Actually, levels of total/specific IgE as well as expression rate of allergic diseases slightly higher than in the general population have already been reported in patients with CSU [ 56 – 58 ]. Moreover, the skin MC TC subset, the main actor of CSU history, largely depends on its multiple and not yet fully clarified functions by activation of FcεRI-IgE axis, among others also by auto-allergens [ 8 – 12 , 25 , 59 , 60 ]. This is all true considering that in experimental animal models it has elegantly been demonstrated that perivascular skin MC TC are able to exhibit a selective uptake of IgE by their positioning and by extending a cell process across the vessel wall to capture intraluminal IgE [ 61 ].…”

“…Although the pathophysiology of CSU is not yet completely understood, a strong characteristic of the disease is the specific increased activation and/or degranulation of skin mast cells (MCs). These are primed to increase the release of proinflammatory and vasoactive mediators through different immunological or non-immunological stimuli and synergistic/sequential different pathomechanisms [ 6 – 12 ]. Over the past five years, clinical studies have demonstrated the efficacy and safety of the monoclonal antibody omalizumab in the treatment of spontaneous and inducible chronic urticaria [ 13 – 15 ].…”

Eradication of Helicobacter pylori , as add-on therapy, has a significant, but temporary influence on recovery in chronic idiopathic urticaria: a placebo-controlled, double blind trial in the Polish population

“…If the followed eradication decrease the symptoms again – the HP diagnosis and eradication can be considered as add-on therapy to standard chronic urticaria diagnosis and treatment. Recently emerging mastocyte/basophil priming phenomenon, as a feature of CIU and consequence of autoreactive IgE against several HP internal factors may provide a new insight into pathogenesis of this complex syndrome [ 34 ].…”

The method to detect sIgE to thyroid peroxidase in cases of the patients with autoimmune and allergic diseases

“…По мере увеличения антигенной нагрузки (при более выраженном воспалительном повреждении ткани) иммунный ответ переключается на IgG. Данные о том, что IgE-аутоантитела, включая sIgE к ТПО, могут индуцировать симптомы ХСК, подтверждаются активацией тучных клеток и базофилов [10,13,14], а также эффективностью терапии омализумабом у пациентов с ХСК [9].…”