• 1 January 1968
    • journal article
    • research article
    • Vol. 14  (6) , 825-+
Abstract
Bacterial [Escherichia coli] endotoxin was injected into rat hind footpads together with bacterial flagellin and 125i_labelled human serum albumin (HSA); the latter was used unmodified or heat denatured (H.HSA) or as an HSA-antibody complex. Endotoxin did not affect the trapping, retention nor localization of the labelled HSA in the popliteal and aortic lymph nodes, whether the antigen was injected as HSA, H.HSA or as an HSA-antibody complex. If endotoxin was injected at the same time as: flagellin, there was an increased production of anti-flagellin antibody; and H.HSA or HSA-antibody complex, detectable amounts of anti-HSA antibody were produced. When H.HSA and endotoxin were injected, the primary response was long lived yet the period of induction of antibody formation and of antigen persistence in the lymphoid tissues was short. If, during the primary antibody response to H.HSA, the animals were challenged with HSA, equally strong secondary antibody responses occurred with an HSA-antibody complex or with HSA alone. The results were interpreted in terms of the tissue localization pattern of H.HSA (medullary macrophage) and HSA-antibody complex (medulla and lymphoid follicles). It was suggested that: induction of antibody formation and priming of cells for a secondary antibody response might occur following localization of the antigen in the medulla and that antigen localization in the lymphoid follicles might not be a strict requirement for this; and the follicular localization of antigen might be the preferential mechanism for the firing of a secondary antibody response.