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Impact of T-Cell Depletion on CMV-Specific Memory T and B Cell Homeostatic Proliferation After Kidney Transplantation.

M. Jarque,2 S. Luque,2 E. Crespo,2 E. Melilli,1 J. Torras,1,2 J. Grinyó,1,2 O. Bestard.1,2

1Kidney Transplant Unit, Bellvitge University Hospital, Barcelona, Spain
2Nephrology Laboratory, IDIBELL, Barcelona, Spain

Meeting: 2017 American Transplant Congress

Abstract number: 30

Keywords: Cytomeglovirus, Induction therapy, Kidney transplantation, T cells

Session Information

Session Name: Concurrent Session: Cutting Edge - Cytomegalovirus

Session Type: Concurrent Session

Date: Sunday, April 30, 2017

Session Time: 2:30pm-4:00pm

 Presentation Time: 3:18pm-3:30pm

Location: E353C

Human CMV infection is the most common opportunistic infection after kidney transplantation, with a negative impact on kidney allograft outcome. Transplant recipients are at higher risk of CMV infection because of immunosuppression, particularly when using T-cell depleting agents such as rabbit anti-thymocyte globulin (rATG). CMV-specific T and B-cell responses are crucial for controlling viral replication. Whether CMV-specific memory T and B cells repopulate after rATG treatment and how they influence on CMV infection has not been well documented yet.

Methods: We evaluated CMV-specific memory T and B cell responses using the IFN-Y and IgG ELISPOT assays. 70 consecutive kidney transplant patients receiving either rATG (n=42) or anti-IL2R monoclonal antibodies (basiliximab®) (n=28) followed by tacrolimus, MMF and steroids. We monitored the kinetics of T and B-cell responses against two dominant CMV antigens (IE-1 and pp65) at baseline, two weeks and at one, three and six months after transplantation and evaluated their impact on CMV infection.

Results: rATG-treated patients showed a generalized abrogation of CMV-sp T-cell frequencies over the first 6 months as compared to basiliximab-treated patients that also showed reduced CMV-sp T-cell frequencies over time. RATG-treated patients showed lower CMV-sp T-cell frequencies at 2 weeks(p<0.05) but fully recovered by months 3 and 6 for pp65 and IE-1, respectively as compared to baseline (P=NS). No impact on CMV-sp T-cell responses was observed regarding the type of preventive strategy used. Notably, patients not recovering sufficient CMV-sp T-cell frequencies more likely developed CMV infection after kidney transplantation. CMV-sp memory B-cell frequencies were not influenced by the use of T-cell depletion nor basiliximab®.

Conclusions: rATG induction significantly impacts on early CMV-sp memory T-cell responses after transplantation, although a rapid CMV-sp T-cell homeostatic proliferation might be observed in some patients thus, driving protection against CMV infection.

CITATION INFORMATION: Jarque M, Luque S, Crespo E, Melilli E, Torras J, Grinyó J, Bestard O. Impact of T-Cell Depletion on CMV-Specific Memory T and B Cell Homeostatic Proliferation After Kidney Transplantation. Am J Transplant. 2017;17 (suppl 3).

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To cite this abstract in AMA style:

Jarque M, Luque S, Crespo E, Melilli E, Torras J, Grinyó J, Bestard O. Impact of T-Cell Depletion on CMV-Specific Memory T and B Cell Homeostatic Proliferation After Kidney Transplantation. [abstract]. Am J Transplant. 2017; 17 (suppl 3). https://atcmeetingabstracts.com/abstract/impact-of-t-cell-depletion-on-cmv-specific-memory-t-and-b-cell-homeostatic-proliferation-after-kidney-transplantation/. Accessed May 18, 2025.

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