Suppression of antibody-mediated accumulation of eosinophils in chronic inflammatory lesions by concomitant delayed hypersensitivity reactions.
Studies were carried out in order to explain the often small contribution of eosinophils to immunologically mediated chronic inflammatory reactions. A chronic inflammation model was used in which large numbers of eosinophils accumulated in the peritoneal injections with PPD or ovalbumin (OA). Eosinophil accumulation could be strongly suppressed by pre-immunization with a mycobacteria-containing adjuvant, which induces delayed hypersensitivity to the stimulating antigen. Suppression of OA-induced eosinophil accumulation could be obtained in a non-specific way by concomitant delayed hypersensitivity reactions to PPD. The absence o eosinophil accumulation was not related to a lack of relevant antibodies. Histological studies suggested that similar numbers of basophils were locally available in both non-pre-immunized and pre-immunized groups to allow for the attraction of eosinophils by the expression of basophil anaphylactic reactivity. Skin tests and macrophage migration inhibition measurements provided further support for the hypothesis that local lymphokine release may suppress the accumulation of eosinophils in chronic inflammatory lesions.
D000818:Animals; D000917:Antibody Formation; D000941:Antigens / Q000276:immunology; D001491:Basophils; D002465:Cell Movement; D002634:Chemotaxis, Leukocyte; D002908:Chronic Disease; D004804:Eosinophils / Q000276:immunology*; D005260:Female; D006968:Hypersensitivity, Delayed; D007958:Leukocyte Count; D051379:Mice; D010538:Peritonitis / Q000276:immunology*; D012882:Skin Tests; D014373:Tuberculin / Q000276:immunology
D000941:Antigens; D014373:Tuberculin