[New perspectives in the modulation of allergic inflammation].
Current studies on IgE-dependent allergic reactions focus on the regulation of IgE synthesis by cellular IgE receptors or by their fragments, so-called IgE-binding factors. Recent studies suggest that lymphokines, such as interleukin-4 (IL-4) and interferon-gamma (IFN-gamma), may be more relevant in the modulation of IgE synthesis. Under this aspect studies should concentrate on the role of anti-isotypical anti-IgE antibodies which can be found frequently in IgE-mediated responses. Further studies have given new insights in the variation of releasability and lymphokine-mediated conditioning of effector cells, depending on the type of allergic reaction. Pretreatment of neutrophils with granulocyte macrophage- colony stimulating factor (GM-CSF), or basophils with interleukin-3 (IL-3) renders these cells capable of producing or releasing inflammatory mediators, such as histamine, leukotrienes or platelet activating-factor (PAF). The fact that the interaction of purified lymphokines, such as IL-3 or IL-8 with basophils causes the release of mediators, indicates a possible mechanism for the induction of immediate and delayed allergic reactions. New insights in these mechanisms may offer new immunopharmacological aspects in the treatment of allergic reactions. IgE-mediated allergic reactions can be divided into two distinct phases. During the period of sensitization allergen exposure causes the production of class E immunoglobulins (IgE) in genetically predisposed persons. Repeated allergen exposure in sensitized persons leads to bridging of IgE molecules with basophils or mast cell membranes which finally causes the production and the release of inflammation mediators, such as histamine, leukotrienes and PAF.(ABSTRACT TRUNCATED AT 250 WORDS)
de Weck
A L
AL
Institut für klinische Immunologie, Bern.
Stadler
B M
BM
Dahinden
C A
CA
D000944:Antigens, Differentiation, B-Lymphocyte / Q000502:physiology*; D001685:Biological Factors / Q000502:physiology; D016207:Cytokines; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology*; D007111:Immunity, Cellular / Q000276:immunology; D007073:Immunoglobulin E / Q000096:biosynthesis*; D008222:Lymphokines / Q000502:physiology; D011961:Receptors, Fc / Q000502:physiology*; D017455:Receptors, IgE
D000944:Antigens, Differentiation, B-Lymphocyte; D001685:Biological Factors; D016207:Cytokines; D008222:Lymphokines; D011961:Receptors, Fc; D017455:Receptors, IgE; D007073:Immunoglobulin E
Neue Perspektiven in der Modulation der allergischen Entzündung.