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Hypersensitivity reactions of the delayed inflammatory tuberculin type are considered to be initiated by an immunological process because they occur only in the specifically sensitized host. Nevertheless, no clear cut relationship between this type of hypersensitivity and conventional serum antibody has been demonstrated, although frequently such circulating antibody is present with its specificity directed against the same substance that can elicit the delayed hypersensitivity reaction. Unlike hypersensitivity of the immediate type, serum from donors showing the delayed type of hypersensitivity does not ordinarily confer sensitivity when injected into non-sensitive recipients.Transfer to normal guinea pigs of delayed sensitivity to simple chemicals and to tuberculin, by means of living leucocytes was first demonstrated using peritoneal exudates from sensitized guinea pigs (Landsteiner and Chase (1); Chase (2)). In man, transfer of delayed sensitivity to tuberculin and to certain streptococcal proteins is readily accomplished by subcutaneous or intradermal injections of white cells from the peripheral blood of sensitive donors into nonsensitive recipients (3, 4). The leucocyte factor involved in transfer may be extracted from the cells by disrupting them by repeated freezing and thawing, and is not destroyed by desoxyribonuclease, ribonuclease (5), or by treatment with crystalline trypsin (6).The nature of the factor or factors responsible for transfer of delayed hypersensitivity in man and their relation to serum antibody are not known. This may be due, in part at least, to the fact that the tuberculin and streptococcal products that have been used as test materials are neither homogeneous nor well defined and that no sensitive method is available for determination of small amounts of specific antibody, even if present.

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