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Published on: May 17, 2015
Posttransplant Immune Activation: Innocent Bystander or Insidious Culprit of Posttransplant Accelerated
Didier Ducloux1,2, Jamal Bamoulid1,2, Thomas Crepin1,2
11 Inserm, UMR1098, Federation Hospitalo-Universitaire INCREASE, Besançon, France.
Insights
Kidney transplant recipients face high cardiovascular risks, partly due to activated CD8+ T cells. These immune cells promote atherosclerosis, contributing to transplant patient mortality.
Area of Science:
- Immunology
- Nephrology
- Cardiology
Background:
- Cardiovascular disease (CVD) is a leading cause of death in kidney transplant patients.
- Traditional cardiovascular risk factors do not fully explain the elevated CVD risk post-transplant.
- Immune system dysregulation after transplantation is a potential contributor to accelerated atherosclerosis.
Purpose of the Study:
- To investigate the role of adaptive immunity, specifically CD8+ T cell activation, in post-transplant atherosclerosis.
- To identify factors contributing to CD8+ T cell expansion in kidney transplant recipients.
- To explore the pro-atherogenic effects of activated CD8+ T cells.
Main Methods:
- Analysis of immune cell populations in kidney transplant recipients.
- Assessment of CD8+ T cell activation and exhaustion markers.
- Correlation of immune findings with clinical factors and cardiovascular events.
Main Results:
- CD8+ T cell activation is a common immune feature in kidney transplant recipients.
- Expansion of exhausted/activated CD8+ T cells is linked to factors like CMV infection and lymphodepletive therapy.
- These activated CD8+ T cells exhibit pro-atherogenic potential.
Conclusions:
- Activated CD8+ T cells represent a significant, potentially modifiable, contributor to accelerated atherosclerosis in kidney transplant patients.
- Understanding the drivers of CD8+ T cell expansion is crucial for mitigating cardiovascular risk.
- Targeting adaptive immune responses may offer novel strategies for preventing CVD post-transplantation.
Abstract:
Cardiovascular disease is a major cause of morbidity, disability, and mortality in kidney transplant patients. Cumulative reports indicate that the excessive risk of cardiovascular events is not entirely explained by the increased prevalence of traditional cardiovascular risk factors. Atherosclerosis is a chronic inflammatory disease, and it has been postulated that posttransplant immune disturbances may explain the gap between the predicted and observed risks of cardiovascular events. Although concordant data suggest that innate immunity contributes to the posttransplant accelerated atherosclerosis, only few arguments plead for a role of adaptive immunity. We report and discuss here consistent data demonstrating that CD8+ T cell activation is a frequent posttransplant immune feature that may have pro-atherogenic effects. Expansion of exhausted/activated CD8+ T cells in kidney transplant recipients is stimulated by several factors including cytomegalovirus infections, lymphodepletive therapy (e.g., antithymocyte globulins), chronic allogeneic stimulation, and a past history of renal insufficiency. This is observed in the setting of decreased thymic activity, a process also found in elderly individuals and reflecting accelerated immune senescence.
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