In Allogeneic transplantations, in most cases, are performed between HLA-matched siblings donors. The alloresponse is directed to minor histocompatibility antigens (miHA) expressed on host tissues. The miHA are processed self-protein degradation products that can be presented in association with either major histocompatibility complex (MHC) class I or class II molecules on host parenchymal and antigen-presenting cells (APC), resulting in stimulation of donor CD4+ and CD8+ T cells, respectively. Studies have shown that either the recipients or donora DCs can present allo-antigens to donor T-cells. Allogeneic donor T cells with the same MHC molecules can thus recognize miHA that is not expressed by themselves. During the process of GVHD, activated donor T-cells migrate to target tissue and induce GVHD via either direct cell contactor (cytotoxic T-cells) or cytokine mediated toxicity (T-helper cells). Our group found that either CD4+ T cells or CD8+ T cells could initiate lethal GVHD independently in Allo-BMT mouse model. Friedman et al. analyzed the T-cell responses after transplantation by CDR3- size spectratyping in B6 --> BALB/C Allo-BMT model. They revealed clonal or oligoclonal expansions of the VÎ² 2, 4, and 6 to 14 families for the CD4+ response and of the VÎ² 4, 6, 8 to 11, and 14 families for the B6 CD8+ response. Appropriate positive selection of these T-cell receptor VÎ²-skewed CD4+ and CD8+ T-cell subsets and their subsequent transfer into lethally irradiated BALB.B recipients resulted in fatal GVHD induction. In contrast, BALB B mice transplanted with non-skewed Vi² T cells survived, with minimal symptoms of GVHD.
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Last date updated on June, 2014