Key result
Tc1 cells drive early graft vasculitis while Tc2 cells promote eosinophil infiltration in murine allografts.
Why the study?
It was unclear whether allospecific CD8+ T cells can mediate rejection of vascularized cardiac allografts without CD4+ T cell help and whether Tc1 and Tc2 subsets differ in rejection capability.
Population
H-2b RAG 1-/- mice receiving fully mismatched H-2d cardiac allografts
Comparison
Adoptive transfer of allo-(H-2d)-reactive Tc1 cells vs Tc2 cells vs unmanipulated controls
Design
Preclinical adoptive transfer study with predefined timepoint analyses
Follow-up
7 days and predefined timepoints
Authors
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Tc1 and Tc2 subsets mediate distinct rejection patterns without CD4 help in mice; leaves open relevance to human allograft rejection.
CD8+ T cell subsets Tc1 and Tc2 can independently mediate murine cardiac allograft rejection in the absence of CD4+ T cells, but they elicit distinct histopathologic forms of rejection.
Delfs et al. (2001) studied Cardiac allograft rejection. Adoptive transfer of allo-reactive Tc1 or Tc2 cells vs. Tc1 vs Tc2 was evaluated on Histopathologic forms of cardiac allograft rejection. Adoptive transfer of Tc1 cells led to early graft vasculitis, whereas Tc2 cells promoted extensive eosinophil infiltration and giant cell formation in a murine cardiac allograft model.
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