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Reduced neointima formation after arterial injury in CD4-/- mice is mediated by CD8+CD28hi T cells
Paul C Dimayuga1, Kuang-Yuh Chyu, Wai Man Lio
1Oppenheimer Atherosclerosis Research Center, Division of Cardiology, Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA. dimayugap@cshs.org
Background:
CD8(+) T-cell activation, characterized by increased CD28 expression, reduces neointima formation after arterial injury in mice. The CD8(+)CD28(hi) phenotype is associated with increased effector function. In this study, we used a mouse model that has CD8(+) but no CD4(+) T cells (CD4-/-) to assess the role of CD8(+) T cells and test the function of CD8(+)CD28(hi) T cells in modulating neointima formation after arterial injury.
Methods And Results:
Neointima formation after pericarotid arterial cuff injury was significantly less in CD4-/- mice compared with wild-type (WT) mice. Negligible baseline lytic activity by splenic CD8(+) T cells from uninjured WT mice against target syngeneic smooth muscle cells was significantly increased 7 days after injury. Interestingly, CD8(+) T cells from uninjured CD4-/- mice had significant lytic activity at baseline that remained elevated 7 days after injury. CD8(+) T-cell lytic activity was significantly reduced by depletion of CD28(hi) cells. CD8(+)CD28(hi) T cells adoptively transferred into recipient Rag-1-/- mice significantly reduced neointima formation compared with CD8(+)CD28(+) T-cell recipient mice.
Conclusions:
CD8(+) T cells reduced neointima formation after arterial injury, attributed in part to increased function of the CD8(+)CD28(hi) phenotype.
