Hybrid resistance modulates the inflammatory process induced by lymphocytic choriomeningitis virus-immune T cells.

The magnitude of the meningitis occurring 72 hr after adoptive transfer of 8-day lymphocytic choriomeningitis (LCMV)-immune effector T cells from cyclophosphamide-treated or untreated donors into cyclophosphamide-suppressed, LCMV-infected recipients is modified by the hybrid histocompatibility (Hh) effect. Evidence of inhibition in (H-2Kd Dd X H-2Kb Db)F1, as compared with H-2Kb Db, recipient mice is found for H-2Kd Db, H-2Kd Db and (H-2Kk Db X H-2Kb Db)F1, but not for (H-2Kk Dk X H-2Kb Db)F1 or H-2Kb Dd, LCMV-immune donor populations. The effect is cell dose-dependent, and the inflammatory process is 2.5-10 times lower in F1 than in recipient mice of parental type. These data indicate that the Hh effect is not directed solely at precursor populations, or at T cells which bear idiotypes reactive to MHC glycoproteins expressed in the F1 recipients. The inflammatory process initiated by fully-functional, LCMV-immune T cells is inhibited in the same way. The fact that the levels of natural killer cell activity in the virus-infected, cyclophosphamide-treated recipients are not much higher than those in normal mice indicates that the operation of hybrid resistance in LCM is not likely to be a special case, and should be taken into account in all T cell transfer systems.