Skip to main content

Table 2 Carbon monoxide immunomodulation during transplantation

From: The immunomodulatory role of carbon monoxide during transplantation

CO TARGET CONSEQUENCES
DONOR ↓Toll-like receptor (TLR)4
↓endothelial cell proliferation
↓lymphocytic infiltration
↓inflammatory cytokines production (IFN-g)
↓apoptosis
↓Reactive oxygen species (ROS)
↓NFκB (IκB degradation)
↓E-selectin/ ICAM-1
GRAFT ↑Hypoxia inducible factor (HIF)-1a
↑Vascular endothelial growth factor (VEGF)
↓apoptosis (↑Bcl-2, ↓Bax, ↓caspase 3)
↓inflammatory cytokines production (TNF, IL-6)
↓prostaglandin (COX2)
↓ICAM-1
↓NFκB
RECIPIENT ↓Ischemia and reperfusion injury
↓fibrosis
↓anti-donor IgG antibodies
↓chemokine receptors (CCR1, CXCR3, CXCR5)
↓chemokines (IL-8, MIP-1a)
↓ICAM-1
↓IL-2 (↓T cell proliferation)
↓leukocyte infiltration (CD3+, CD4+, CD8+ T cells and macrophages)
↓macrophage activation (↓MHC class II)
↓neutrophil activation (↓MPO)
↓apoptosis (↓CD95/FasL)
↓inflammatory cytokines production (IL-1β, TNF)
↓iNOS
↓prostaglandin (COX2)
↓platelet aggregation
↑cell cycle inhibition (↑p21clip1)
↑Treg (Foxp3+ T cells)