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Anti CD45RB Antibody Therapy Attenuates Renal Ischemia Reperfusion Injury by Inducing Regulatory B Cells

S. Lee1, S. Park1, J. Hwang1, J. Ryu2, T. Koo2, C. Ahn2, J. Yang3

1Biomedical Research Institute, Transplantation Center, Seoul National University Hospital, Seoul, Korea, Republic of, 2Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea, Republic of, 3Department of surgery, Seoul National University Hospital, Seoul, Korea, Republic of

Meeting: 2019 American Transplant Congress

Abstract number: 80

Keywords: Antibodies, B cells, Ischemia, Renal ischemia

Session Information

Date: Sunday, June 2, 2019

Session Name: Concurrent Session: Ischemia Reperfusion & Organ Rehabilition I

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

 Presentation Time: 3:30pm-3:42pm

Location: Room 313

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*Purpose: Regulatory B cells (Bregs) are a new B cell subset that suppresses immune responses. Recently, both anti-CD45RB and anti-Tim-1 treatments have been found to regulate immune responses by inducing Bregs; however, the role of Bregs in renal ischemia-reperfusion injury (IRI) has not been shown.

*Methods: We investigated impacts of Bregs and anti-CD45RB on IRI and its mechanisms using mouse models of bilateral renal IRI.

*Results: Adoptive transfer of Bregs prior to or following IRI attenuated renal IRI. Anti-CD45RB treatment showed better renoprotective effects against IRI than anti-Tim-1 treatment. Anti-CD45RB treatment with or without anti-Tim-1 prior to IRI increased the renal infiltration of CD19+Tim-1+ Bregs and regulatory T cells. Anti-CD45RB decreased serum creatinine levels, pathologic injury score, and tubular apoptosis. Levels of IL-1β, IL-6, MCP-1, IFN-γ, and IL-17 were decreased, whereas IL-10 was increased in the CD45RB group. Following IRI, anti-CD45RB with or without anti-Tim-1 also induced Bregs, thereby improving renal function and tubular regeneration. In RAG1 knockout mice with B cell transfer, TCRα knockout mice, and wild-type mice with T cell depletion, anti-CD45RB increased Bregs and attenuated IRI. However, anti-CD45RB did not attenuate IRI in RAG1 knockout mice with T cell transfer or μMT mice and induced only mild improvement in wild-type mice with B cell depletion. Furthermore, B cells from IL-10 knockout mice did not show anti-CD45RB-mediated renal protection against IRI, in contrast to those from wild-type mice.

*Conclusions: Anti-CD45RB treatment attenuated acute renal injury and facilitated renal recovery after IRI through induction of IL-10+ Bregs. The present study suggests anti-CD45RB as a potential therapeutic strategy in renal IRI.

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To cite this abstract in AMA style:

Lee S, Park S, Hwang J, Ryu J, Koo T, Ahn C, Yang J. Anti CD45RB Antibody Therapy Attenuates Renal Ischemia Reperfusion Injury by Inducing Regulatory B Cells [abstract]. Am J Transplant. 2019; 19 (suppl 3). https://atcmeetingabstracts.com/abstract/anti-cd45rb-antibody-therapy-attenuates-renal-ischemia-reperfusion-injury-by-inducing-regulatory-b-cells/. Accessed January 24, 2021.

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