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Published on: May 2, 2013
Antithymocyte globulins in renal transplantation-from lymphocyte depletion to lymphocyte activation: The
Jamal Bamoulid1, Thomas Crépin1, Cécile Courivaud1
1CHU Besançon, Department of Nephrology, Dialysis, and Renal Transplantation, F-25030 Besançon, France; UMR1098, Federation hospitalo-universitaire INCREASE, Besançon F-25020, France; Université de Franche-Comté, Faculté de Médecine et de Pharmacie, Besançon F-25020, France; Structure Fédérative de Recherche, SFR FED4234, Besançon F-25000, France.
Compelling data suggest that lymphocyte depletion following T cell depleting therapy may induce prolonged CD4 T cell lymphopenia and trigger lymphocyte activation in some patients. These profound and non-reversible immune changes in T cell pool subsets are the consequence of both impaired thymic renewal and peripheral homeostatic proliferation. Chronic viral challenges by CMV play a major role in these immune alterations. Even when the consequences of CD4 T cell lymphopenia have been now well described, recent studies shed new light on the clinical consequences of immune activation. In this review, we will first focus on the mechanisms involved in T cell pool reconstitution after T cell depletion and further consider the clinical consequences of ATG-induced T cell activation and senescence in renal transplant recipients.
Compelling data suggest that lymphocyte depletion following T cell depleting therapy may induce prolonged CD4 T cell lymphopenia and trigger lymphocyte activation in some patients. These profound and non-reversible immune changes in T cell pool subsets are the consequence of both impaired thymic renewal and peripheral homeostatic proliferation. Chronic viral challenges by CMV play a major role in these immune alterations. Even when the consequences of CD4 T cell lymphopenia have been now well described, recent studies shed new light on the clinical consequences of immune activation. In this review, we will first focus on the mechanisms involved in T cell pool reconstitution after T cell depletion and further consider the clinical consequences of ATG-induced T cell activation and senescence in renal transplant recipients.
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