Mechanisms of Allergic Inflammation and IgE Analysis in Clinical Practice

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Laboratorinė medicina. 2011,
t. 13,
Nr. 1,
p. 31 -

Mechanisms of Allergic Inflammation and IgE Analysis in Clinical Practice

Regina Emužytė, Ingrida Pumputienė, Regina Firantienė


Allergic inflammation is most important in the development of allergic diseases. All allergic reactions according to their immunologic mechanism are classified into four basic types. Type I allergic reac­tions (atopic diseases) are a major health problem. IgE sensitization against aller­gens increased up to 50% together with an increase in allergic disease up to 30% in the popul ation. S. G. O. Johansson in Sweden, K. Ishizaka and T. Ishizaka in the United States in 1966 simulta­neously discovered immunoglobulin E and its role in the triggering of allergic re­actions. The pathophysiology of allergic disease is multifactorial involving an in­tricate network of interactions among cells, mediators and especially cytokines. In atopic subj ects all ergen induces acti­vation and/or proliferation of cells having the Th2 cytokine profile. Expression of Th2 cytokines is critical in the induction of IgE synthesis. IL-4 plays the most cru­cial role as a switching factor of B cells from IgM/IgG to the IgE antibody iso­type. Acute phase of type I reaction is di­rectly associated with mast cell aclivaf tion, preformed active mediators as his­tamine and lipid mediators. Late (inflam­matory) phase of type I reaction is mainly induced by cytokines and directly associ­ated with eosinophil activation. Late phase is clearly important in the develop­ment of chronic allergic disease. Changes in the balance between allergen-specific T-Reg cells and Th2 and/or Th1 cells are crucial in the development of allergic dis­eases. Investigations of immunological mechanisms in allergic inflammation are important for more effective diagnostics, prevention and therapy of allergy.

Keywords: allergy, classification, aller­gic inflammation, mediators, cytokines, IgE, mast cell, eosinophil, Th2 cell.


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