No abstract

Delayed-onset erythematous skin reactions elicited in adult guinea pigs sensitized with protein antigens in incomplete Freund's adjuvant have been called "Jones-Mote" reactions to differentiate them from classic tuberculin type delayed hypersensitivity (1). However, this distinction has depended on relatively minor gross and microscopic differences and on the fact that JonesMote reactions, in contrast to delayed hypersensitivity, may be elicited only at early intervals after sensitization (2, 3). It is not surprising, therefore, that many workers have regarded Jones-Mote reactivity as a weak expression of delayed hypersensitivity (4).We have previously presented immunochemical and biologic data which permit a further distinction between Jones-Mote and classic delayed hypersensitivity reactions (5, 6). The two categories of reaction were shown to have different carrier requirements for hapten-specific sensitization but similar requirements for the expression of skin test reactivity. It was suggested that both reactions involve sensitized lymphoid cells, and that Jones-Mote reactions do not represent a combination of antigen with preformed antibody.We here demonstrate that Jones-Mote reactions have a unique light and electron microscopic morphology which is characterized by the accumulation of large numbers of basophilic leukocytes in the dermis. We prefer to designate

Delayed (cell-mediated) hypersensitivity reactions have been regarded by most workers as a qualitatively homogeneous group (1-3), although well-recognized quantitative differences occur depending primarily on mode of immunization. Classic tuberculin-type delayed hypersensitivity is typically produced by the injection of antigen in complete Freund's adjuvant or in other mixtures containing products of the tubercle bacillus; similar reactivity occurs after dermal contact with simple chemicals and after infections (mycobacterial, fungal, and viral). Delayed-onset skin reactivity can also be produced transiently in a variety of soluble proteins by injection of antigen-antibody complexes or small amounts of the antigen intradermally without mycobacterial adjuvant (4, 5). The latter type of delayed hypersensitivity was termed "Jones-Mote" reactivity by Raffel and Newel (6), who considered it to be qualitatively different from classic delayed hypersensitivity and resembling more closely reactions seen, by those investigators, in humans (7). In the guinea pig, both types of delayed hypersensitivity give a maximum skin reaction at 24 hr, are not necessarily associated with circulating antibody, and can be passively transferred by cells but not by serum (5). Jones-Mote reactivity occurs early in immunization and is evanescent, waning with the appearance of circulating antibody, in contrast to classic delayed hypersensitivity which persists and increases with time. Histologic studies in the past (8-10) have in general shown only quantitative differences between classic delayed and J ones-Mote hypersensitivity reactions, and most investigators have felt the latter to be a weak form of the delayed reaction.The question of whether the two types of delayed-onset hypersensitivity involve similar or qualitatively different mechanisms was studied using the