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Long-Term Islet Xenograft Survival Requires Effective Control of Early Xenogeneic IL-17 Response and Late Xenogeneic IFN-γ Response.

H. Kang,1 S. Wang,2 X. Zhang,3 A. Singh,5 L. Zhang,1 W. Suarez-Pinzon,5 S. Miller,4 B. Hering,5 X. Luo.1,3,4

1Medicine, Northwestern University, Chicago, IL
2Surgery, Tianjin Union Medical Center, Tianjin, China
3Comprehensive Transplant Center, Northwestern University, Chicago, IL
4Microbiology and Immunology, Northwestern University, Chicago, IL
5Schulze Diabetes Institute, University of Minnesota, Minneapolis, MN.

Meeting: 2016 American Transplant Congress

Abstract number: B38

Keywords: Islets, Xenotransplantation

Session Information

Date: Sunday, June 12, 2016

Session Name: Poster Session B: Allograft Rejection, Tolerance, and Xenotransplantation

Session Time: 6:00pm-7:00pm

 Presentation Time: 6:00pm-7:00pm

Location: Halls C&D

Related Abstracts
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Introduction: Tolerance induction for xenogeneic islet transplant remains a challenge. We have previously shown that peri-transplant infusion of donor cells treated with 1-ethyl-3-(3'-dimethylaminopropyl)-carbodiimide (ECDI) is effective in inducing long-term allograft protection. The current study tested the efficacy and mechanisms of this therapy in discordant xenogeneic islet transplantation.

Method: ECDI-treated porcine splenocytes (SP) were infused to B6 mice at day -7, +1. 3,000 IEQ of porcine islets were transplanted in B6 mice on day 0.

Results: In this model, we found that donor-stimulated IL-17 production played a prominent role in the early rejection of porcine islets. The anti-donor IL-17 response was induced by both direct and indirect stimulation, and was seen in both CD4 and CD8 compartments. Recipient treatment with donor porcine ECDI-SP significantly reduced anti-donor IL-17, however by itself did not provide significant protection (MST = 12 days). Interestingly, rejecting porcine islet xenografts were heavily infiltrated with B220+ B cells, and transient depletion of B cells extended islet xenograft survival (MST = 45 days). When we further added a short course of rapamycin (1mg/kg, day -8 to +10), the resulting triple therapy led to long-term (> 100 days) graft survival in ~65% recipients. The protection provided by the triple therapy correlated with sustained inhibition of anti-donor IL-17 response. However, recipients with islet xenograft survival >100 days experienced late rejection between 100 – 200 days. The late rejection coincided with the emergence of robust anti-donor IFN-γ response and extensive B cell infiltration in the graft, although a complete absence of anti-xenogeneic antibodies.

Conclusions: Early rejection of discordant islet xenografts is predominantly driven by anti-donor IL-17 response, whereas late rejection in triple therapy treated recipients is driven predominantly by anti-donor IFN-γ response and possibly graft-infiltrating B cells exerting a direct graft effect beyond their capacity in xenogeneic antibody production.

CITATION INFORMATION: Kang H, Wang S, Zhang X, Singh A, Zhang L, Suarez-Pinzon W, Miller S, Hering B, Luo X. Long-Term Islet Xenograft Survival Requires Effective Control of Early Xenogeneic IL-17 Response and Late Xenogeneic IFN-γ Response. Am J Transplant. 2016;16 (suppl 3).

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To cite this abstract in AMA style:

Kang H, Wang S, Zhang X, Singh A, Zhang L, Suarez-Pinzon W, Miller S, Hering B, Luo X. Long-Term Islet Xenograft Survival Requires Effective Control of Early Xenogeneic IL-17 Response and Late Xenogeneic IFN-γ Response. [abstract]. Am J Transplant. 2016; 16 (suppl 3). https://atcmeetingabstracts.com/abstract/long-term-islet-xenograft-survival-requires-effective-control-of-early-xenogeneic-il-17-response-and-late-xenogeneic-ifn-response/. Accessed January 27, 2021.

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