Graft rejection – endogenous or allogeneic?

摘要: The presence and persistence of alloantigen is necessary for graft-specific T-cell-mediated immunity. However, specificity comprises only a single facet an extremely complex process. Evidence accruing to suggest that immunogenicity could be manipulated by endogenous ligands released during tissue injury. Stress molecules are significantly up-regulated following transplantation stimulate conserved receptors on range leucocytes, including dendritic cells (DCs). DCs essential co-stimulation the induction adaptive signals can act as adjuvant leading DC maturation activation. stimulated endogens exhibit enhanced presentation, production pro-inflammatory cytokines, such interleukin-1β (IL-1β) IL-18. Inflammasomes have major role in IL-1β/IL-18 secretion, endogens. Importantly, polarization toward inflammatory T helper type 17 opposed regulatory dependent upon, among other factors, IL-1β. This highlights important differentiation pathway may influenced signals. Minimizing graft damage stress expression should hypothetically advantageous, we feel this area warrants further research, provide novel treatment modalities with potential clinical benefit.