Immune deviation in the mouse: transfer of selective depression of the contact sensitivity and interleukin-2 response with retention of interferon-gamma production requires CD8+ T cells.

Mice were injected intravenously (i.v.) with trinitrophenyl (TNP)-modified spleen cells. They were subsequently immunized by epicutaneous application of 2,4,6-trinitrochlorobenzene (TNCB, picryl chloride) or 'oxazolone'. The intravenous injection of antigen caused immune deviation (split tolerance) with selective loss of contact sensitivity (CS) and antigen-induced interleukin-2 (IL-2) production, and concomitant retention of antigen-induced interferon-gamma (IFN-gamma) production. This phenomenon was antigen specific as the response to oxazolone was unaffected. Moreover, lymph-node cells stimulated with antigen three times in vitro (from 'deviated' mice which had been injected with antigen i.v., and then sensitized with TNCB) showed limited proliferation. The per cent of IL-2R+ cells and the absolute number of V beta 8+ cells dropped. In contrast, lymph-node cells from 'undeviated' mice showed increased proliferation and IL-2 production on repeated stimulation with antigen in vitro and the per cent of IL-2R+ cells and the absolute number of V beta 8+ cells recovered increased. Spleen cells, taken from mice 3-7 days after the injection of antigen i.v., transferred immune deviation to normal recipients i.e. following epicutaneous immunization with TNCB, the recipients showed the same selective unresponsiveness as the donors. Thy-1+ CD4- CD8+ cells were required. These findings indicate that immune deviation can be demonstrated at the level of lymphokine production.