Abstract
When mice have been rendered anergic by a large intravenous dose of sheep erythrocytes, their inability to mount a delayed-type hypersensitivity (DTH) reaction is not due to an absence of mediator cells, for these can be detected in the spleen by cell transfer. Nor is it due to disappearance of accessory cells (monocytes) from circulation. The serum of anergic mice contains blocking factors which are more abundant after absorption with antigen. Such factors are unable to inactivate the mediators of DTH in vitro, nor do they suppress a DTH reaction when introduced locally into the reaction site. They are active, however, when given intravenously to systemically sensitized mice, provided that the sensitized animal has an intact spleen. If the spleen has been removed or the recipients of sensitized cells have been treated with cyclophosphamide before cell transfer, blocking factors are no longer able to suppress a DTH reaction. Reasons are given for the belief that suppression of DTH in animals undergoing a vigorous antibody response is due to the diversion of reactive cells from circulation to undertake an alternative role in antibody formation in the spleen.