Abstract
IgE and not IgG is usually associated with allergy. IgE lodged on mast cells in skin or gut and basophils in the blood allows for the prolonged duration of allergy through the persistent expression of high affinity IgE receptors. However, many allergic reactions are not dependent on IgE and are generated in the absence of allergen specific and even total IgE. Instead, IgG plasma cells are involved in induction of, and for much of the pathogenesis of, allergic diseases. The pattern of IgG producing plasma cells in atopic children and the tendency for direct or further class switching to IgE are the principle factors responsible for long‐lasting sensitization of mast cells in allergic children. Indirect class switching from IgG producing plasma cells has been shown to be the predominant pathway for production of IgE while a Th2 microenvironment, genetic predisposition, and the concentration and nature of allergens together act on IgG plasma cells in the atopic tendency to undergo further immunoglobulin gene recombination. The seminal involvement of IgG in allergy is further indicated by the principal role of IgG4 in the natural resolution of allergy and as the favourable immunological response to immunotherapy. This paper will look at allergy through the role of different antibodies than IgE and give current knowledge of the nature and role of IgG antibodies in the start, maintenance and resolution of allergy.
Highlights
IgE and not immunoglobulin G (IgG) is usually associated with allergy
Immature B cells may switch more directly from IgM to IgE secretion when exposed to certain allergen conformations in early infancy and the suggestion that early exposure to allergens accounts for higher rates of IgE class switching in atopic and allergic children
Most allergens are internalized by antigen-presenting cells, including B-2 cells in germinal centers, macrophages, and dendritic cells, and digested to form peptide fragments expressed on surface MHC class II molecules
Summary
IgE and not IgG is usually associated with allergy. Allergic sensitization is conventionally thought of as the establishment of a population of IgE making plasma cells which induce the degranulation of vasoactive amines from gut, skin, or lung mast cells and blood basophils and cationic proteins from eosinophils. The initial allergic symptoms may originate from the pathogenesis of IgG producing B cell clones to allergens. The frequency of B cells in allergic children switching from IgG to IgE production may be the critical difference in atopic children that enables priming of mast cells and basophils. Scott-Taylor et al. IgG4 is unstable and mops up antigen in blood as a monovalent protein, there is reduced free allergen to stimulate IgE on sensitized mast cells and basophils. Allergic reactions involve a large number of factors and the formation of allergic conditions involves IgG in the establishment of atopy, the generation of clinical symptoms of allergy and in the amelioration of the response and resolution of allergy. The pattern of IgG producing plasma cells in atopic children and the tendency for direct or further class switching to IgE are the seminal events that generate long-lasting sensitization of mast cells in allergic children. This paper will look at allergy through the role of antibodies other than IgE and give current knowledge of the nature and role of IgG antibodies in the start, maintenance, and resolution of allergy
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