Novel approaches to immunotherapy: epitopes, determinants, activators, or modulators?
The immunological mechanism through which immunotherapy (IT) acts is not certainly known. The participation of the so-called "blocking antibodies" has not been proved and how it intervenes in the regulation of the production of IgE is still to be cleared, as it affects the action of lymphocytes Th1 and Th2. Nowadays, IT is based in the concept that the allergic reaction is somehow an antigen (allergen)-antibody (reagin) reaction. The possible modifications of IT are also based on the possibility to interfere in the antigen-antibody interaction. It has been proved in vitro that aqueous extracts of some allergens produce the consumption of complement, by its usual via, in which the C1 component is involved, without the mediation of antibodies, generating anaphylotoxin C3a, which is a powerful releaser of histamine, as well as C3b, which participates in the regulation of the cellular immunitary system. The term atopen should therefore be used when referring to the unspecific activation or adjuvant activity of antigenically different allergens, due to their common structural or functional characteristics. The term allergen should then be used when describing those structural traits of the carrier molecule, which preferently produces the induction, and possible recognition of IgE antibodies. The action atopen and allergen as separate characteristics of a same molecule could theoretically become important in the future of therapeutics. The receptor of membrane CD21 for C3b, in B cells is a link for lectine CD23 of lymphocytes B, which has been identified with the low affinity receptor IgE (Fce RII-CD23). In summary, the basic defect in atopy may reside in a defect of the receptor portion of reagin for atopen, but not in IgE. This means that in the nearby future, this fact should be taken into account in the search of drugs which participate in this kind of activation of allergic reaction, trying to modify or modulate the low affinity receptor IgE or even the high affinity receptor IgE.
Berrens
L
L
CBF. Leti, SA, Madrid, Spain.
D000276:Adjuvants, Immunologic; D000485:Allergens / Q000276:immunology; D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology; D003888:Desensitization, Immunologic / Q000379:methods / Q000639:trends; D000939:Epitopes / Q000276:immunology; D005544:Forecasting; D006801:Humans; D007167:Immunotherapy / Q000379:methods* / Q000639:trends; D016233:Immunotherapy, Active; D051379:Mice; D018448:Models, Immunological; D017464:Receptors, Complement 3d / Q000276:immunology; D017455:Receptors, IgE / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology; D009626:Terminology as Topic; D014944:World Health Organization
D000276:Adjuvants, Immunologic; D000485:Allergens; D000939:Epitopes; D017464:Receptors, Complement 3d; D017455:Receptors, IgE