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.
D000818:Animals; D000956:Antigens, Viral / Q000276:immunology*; D003520:Cyclophosphamide / Q000494:pharmacology; D006648:Histocompatibility; D007116:Immunization, Passive; D007694:Killer Cells, Natural / Q000276:immunology; D008216:Lymphocytic Choriomeningitis / Q000276:immunology*; D008217:Lymphocytic choriomeningitis virus / Q000276:immunology*; D051379:Mice; D008815:Mice, Inbred Strains; D013601:T-Lymphocytes / Q000276:immunology*
D000956:Antigens, Viral; D003520:Cyclophosphamide