Localization of leucocytes in sites of delayed-type hypersensitivity and in lymph nodes: dependence on vasoactive amines.

Murine delayed-type hypersensitivity (DTH) reactions and the localization of 51chromium-labelled leucocytes into DTH sites, as well as into lymph nodes, can be markedly inhibited by drugs that deplete vasoactive amines (VAA; reserpine); antagonize VAA action (methysergide, cyproheptadine), or block the release of VAA from mast cells (Proxicromil). These drug treatments have much less of an effect on the cells that localize in tissues that are not separated from the blood by venule endothelium such as spleen, liver and the bone marrow. These results suggest that localization of many blood borne leucocytes in tissues that are separated from the blood by venule endothelium requires VAA to induce the formation of 'gaps' between the endothelial cells in order for the leucocytes to make an exit from the blood. Thus DTH may be considered, at least in part, as a tissue equivalent of a lymph node 'trap', with the difference being the type of recruited or 'trapped' cell type; inflammatory leucocytes in DTH responses and lymphocytes in lymph nodes.