Key result
CD40 ligand deficiency increases intimal thickening ~3-fold after carotid injury in mice.
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Immune-mediator CD40 ligand is expressed on a variety of cell types involved in the immune response and on the cells of the vascular system. Inhibition of CD40 signaling has been associated with reduction of experimental atherosclerosis and transplant-associated vasculopathy. Immune response also plays a cardinal role in intimal thickening after acute arterial-wall injury. After carotid artery injury in CD40 ligand knockout (CD40L(-/-)) mice, the intimal thickening was increased 3-fold compared with the thickening in background B6/129 mice. The extent of thickening was similar to the thickening in B6/129 mice depleted of T lymphocytes with anti-CD4 and anti-CD8 antibodies. Injection of splenocytes from B6/129 mice into the CD40L(-/-) mice reduced the intimal thickening to the level comparable to the thickening in background B6/129 mice. These data suggest that CD40 signaling plays a significant role in the inhibitory effect of T lymphocytes on intimal thickening after arterial injury.
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Remškar et al. (2001) studied Acute carotid artery injury / intimal thickening. CD40 ligand knockout (CD40L(-/-)) and splenocyte injection vs. Background B6/129 mice (with or without T-lymphocyte depletion using anti-CD4 and anti-CD8 antibodies) was evaluated on Intimal thickening after carotid artery injury (3-fold increase). CD40 ligand deficiency in mice increased intimal thickening 3-fold after carotid artery injury compared with background B6/129 mice, an effect reversed by B6/129 splenocyte injection.
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