STUDIES ON DELAYED CUTANEOUS INFLAMMATORY REACTIONS ELICITED BY INOCULATION OF HOMOLOGOUS CELLS INTO HAMSTERS' SKINS

The intracutaneous inoculation of lymph node cell suspensions from normal hamsters into normal, homologous hosts causes the development of delayed inflammatory reactions, normal lymphocyte transfer (NLT) reactions, the intensities of which reflect the antigenic disparity between donor and recipient. The immunogenetic situations in which they occur indicate that these reactions are due to sensitization in situ on the part of inoculated immunologically competent cells against alien antigens of the host. They are graft versus host reactions. If hamsters are sensitized by cellular or solid tissue homografts and then challenged intracutaneously with lymphoid or epidermal cells from the donor strain, direct reactions are provoked. A positive correlation exists between the development of transplantation immunity and the capacity to give direct reactions. The sensitivity responsible for direct reactions can be suppressed by irradiation or administration of cortisone, and it is transferable by means of viable lymphoid tissues or cells but not by means of serum. Intracutaneous inoculation of viable node or splenic cells from specifically sensitized hamsters into hosts of the donor strain incites transfer reactions, the intensities of which depend upon the number of cells transferred and the level of sensitivity in the animal that provided them. These reactions are not incitable by thymocytes, by killed lymphoid cells, or by serum. Transfer reactions differ from NLT reactions only on a quantitative and chronologic basis. However, a sharp experimental distinction can be drawn between them. For example, if normal MHA node cells and node cells from MHA hamsters sensitized against CB antigens are injected into the skins of MHA's tolerant of CB tissue, only the sensitized cells incite reactions. Both direct and transfer reactions are highly specific immunologically. The inability of node cells to incite NLT or transfer reactions in heavily irradiated hosts and other findings sustain the thesis that it is host cells of hematologic origin, rather than indigenous skin cells, that contribute the antigenic stimulus required for these reactions. All the findings presented are consistent with the hypothesis that the various delayed inflammatory reactions described are manifestations of immunological responses on the part of immunologically competent cells against alien transplantation antigens.