title: Alloantibody and transferable suppressor activity induced by cyclosporine and blood transfusions in the rat.
abstract: The effect of cyclosporine on the alloantibody response to blood transfusion was investigated in inbred strains of rats by IHA and CELISA; recipient animals differed from the donors at the class I (RT1A) or both class I and class II (RT1B) antigens of the major histocompatibility complex. Alloantibody titers stimulated in high responder PVGu/c animals by blood transfusions were attenuated by cyclosporine; this effect was not demonstrated in low responder PVGc rats, as alloantibody titers decreased after further blood transfusions whether or not cyclosporine was given. Cyclosporine not only reduced the initial IgM response but suppressed the subsequent production of IgG. Splenocytes from rats receiving cyclosporine and blood transfusions from donors that differed from the recipients at the class I antigen were effective in suppressing the subsequent antibody response to blood transfusion. When blood transfusions from donors which differed from the recipients at both class I and class II antigenic loci were given after splenocyte transfer, a greater degree of immunosuppression was detected than if the transfusion donor differed only at the class I locus. These data suggest that the sensitization produced by blood transfusions and the persistence or decline of the alloantibody response depend upon the responder status of the recipient. Blood transfusions given with cyclosporine are capable of inducing suppressor activity that is transferable in spleen homogenates. Subsequent alloantibody responses are influenced by the class I and class II disparities of the donor and recipient animals. If these results can be extrapolated to clinical practice, cyclosporine should be given with pretransplant blood transfusions to prevent sensitization, and the transfusion donor should differ from the recipient at both class I and class II antigenic loci.
authors.affiliation: Department of Medicine and Therapeutics, Aberdeen Royal Infirmary, Scotland.
authors.forename: M C
authors.initials: MC
authors.lastname: Jones
authors.forename: D A
authors.initials: DA
authors.lastname: Power
authors.forename: C
authors.initials: C
authors.lastname: Cunningham
authors.forename: K N
authors.initials: KN
authors.lastname: Stewart
authors.forename: G R
authors.initials: GR
authors.lastname: Catto
mesh_terms: D000818:Animals; D001803:Blood Transfusion; D003524:Cyclosporins / Q000494:pharmacology*; D006082:Graft Enhancement, Immunologic; D006649:Histocompatibility Antigens / Q000276:immunology*; D007108:Immune Tolerance / Q000187:drug effects*; D007116:Immunization, Passive; D007074:Immunoglobulin G / Q000096:biosynthesis; D007075:Immunoglobulin M / Q000096:biosynthesis; D007518:Isoantibodies / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains / Q000276:immunology; D013154:Spleen / Q000637:transplantation; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000637:transplantation*
chemical_list: D003524:Cyclosporins; D006649:Histocompatibility Antigens; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007518:Isoantibodies; C038353:histocompatibility antigens RT, rat