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T Hubscher

Publications and source records attributed to T Hubscher.

9 recordsLinked to original sources

Immune and biochemical mechanisms in the allergic disease of the upper respiratory tract; role of antibodies, target cells, mediators and eosinophils.

The pathways leading to the development of the allergic state and subsequently to the characteristic inflammatory response are complex in nature and result from an interplay between immunologic and biochemical events. Along these pathways a number of intrinsic factors, i.e., handling of antigens at mucosal level, transient immunodeficiency states, especially in the secretory IgA system, impairment in the IgE regulatory mechanism, modulation of cyclic nucleotides leading to mediator release and a "feedback" inhibition control provided by histamine and eosinophil derived products greatly dictate the outcome of events associated with allergic inflammation.

Allergens↗

Role of the eosinophil in the allergic reactions. I. EDI-an eosinophil-derived inhibitor of histamine release.

An inhibitor of histamine release was found to be associated with the human eosinophilic leukocyte. This eosinophil-derived inhibitor (EDI) was released from eosinophil-rich fractions upon sonication or interaction with immune reactants (specific allergens or anti-IgE). EDI was found to exert its inhibitory action at the target cell level by increasing the intracellular levels of cyclic-AMP. Preliminary electron microscopic studies show the presence of IgE on the eosinophilic leukocyte and it is suggested that the allergen or anti-IgE-induced release of EDI might be due to a direct interaction of these immune reactants with the eosinophil-bound IgE antibody. The results also suggest that by virtue of liberating a histamine release inhibitor such as EDI, the eopsinophil assumes a modulating role in the allergic inflammatory reaction.

Animals↗

Role of the eosinophil in the allergic reactions. II. Release of prostaglandins from human eosinophilic leukocytes.

Human eosinophilic leukocytes respond to a variety of stimuli by liberating an inhibitor of histamine release. The active principle(s) in this eosinophil-derived inhibitor (EDI) was found to be a mixture of acidic lipids of similar physiocochemical behavior and biologic activity to prostaglandins E1 and E2. Indomethacin, an inhibitor or prostaglandin synthesis, specifically blocked the immune release of EDI. The results indicate that stimulation of human eosinophilic leukocytes results in synthesis and release of prostaglandins E1 and E2 from these cells. These findings strongly support the hypothesis that the eosinophil assumes a modulatory role in the allergic inflammatory reaction. The ways by which, under specific antigenic (allergenic) stimulation, human eosinophils could modulate the events asssociated with the allergic response, through the released prostaglandins, are discussed.

Adenosine Diphosphate↗