Abstract
Raft-versus-host disease (GVHD) is known to be an extremely complex alloantigenic reaction. 1 In our work, we intended to analyze the contribution of RT1 and non-RT1 genetic factors to the course and features of the disease. We used separate lymph node (LN) cells and splenocyte suspensions to induce systemic GVHD in a fully (RT1 and multiple non-RT1) semiallogeneic P→F 1 model with BN. Lx and SHR strains as donors. Recently, a similar model with mixed lymphoid cell inoculum has been exploited for the testing of immunomodulating effects of a new acyclic adenine nucleotide analog. 2,3 These strain combinations are particularly useful when considering the possibility of demonstrating the role of genes of non-RT1 genetic background by inducing GVHD in F 1 (SHR × BN. Lx) hybrids with lymphoid cells originating from individual recombinant inbred (RI) strains of BXH and HXB sets derived from (BN. Lx × SHR)F 2 and (SHR × BN. Lx)F 2 crosses. 4,5
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