Use of antibody induction in pediatric renal transplantation

Pescovitz, Mark D.

doi:10.1097/mot.0b013e328310b0ba

Cited by 9 publications

(1 citation statement)

References 24 publications

(28 reference statements)

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“…However, these in vitro results may not accurately reflect Treg responsiveness in vivo, as previously reported for Treg proliferative capacity [28]. No autoimmune disorders have so far been observed in our series of pediatric transplant recipients, and none have been reported in other series of pediatric transplant recipients who received basiliximab during induction therapy [29], [30]. Accumulating evidence points to a role of Tregs in immune tolerance of allergens [31].…”

Section: Resultsmentioning

confidence: 60%

CD25 Appears Non Essential for Human Peripheral Treg Maintenance In Vivo

et al. 2010

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BackgroundIL-2 has been reported to be critical for peripheral Treg survival in mouse models. Here, we examined Treg maintenance in a series of paediatric liver transplant recipients who received basiliximab, a therapeutic anti-CD25 monoclonal antibody.Methodology/Principal FindingsFoxP3+ CD4 T cells were analyzed by flow cytometry before liver grafting and more than 9 months later. We found that in vivo CD25 blockade did not lead to Treg depletion: the proportion of FoxP3+ cells among CD4 T cells and the level of FoxP3 expression were both unchanged. IL-2Rβ expression was enhanced in FoxP3+ cells both before and after basiliximab treatment, while the level of IL-2Rγ expression was similar in Tregs and non-Tregs. No significant change in the weak or absent expression of IL-7Rα and IL-15Rα expression on FoxP3+ cells was observed. Although the proportion of FoxP3+ cells among CD4 T cells did not vary, food allergies occurred more rapidly after liver grafting in patients who received basiliximab, raising questions as to Treg functionality in vivo in the absence of functional CD25.ConclusionsCD25 appears non essential for human Treg peripheral maintenance in vivo. However, our results raise questions as to Treg functionality after therapeutic CD25 targeting.

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