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Administration of IL-33 Before Allogeneic Stem Cell Transplantation Expands Recipient Treg That Prevent Graft- vs. Host Disease.

B. Matta,1 D. Reichenbach,2 X. Zhang,1 B. Koehn,2 L. Mathews,1 C. Feser,2 M. Smith,2 Q. Liu,1 R. Zeiser,3 B. Blazar,2 H. Turnquist.1

1Dept of Surgery and Starzl Transplant Inst, Univ of Pittsburgh Sch of Med, Pittsburgh, PA
2Dept of Pediatrics, Univ of Minnesota, Minneapolis, MN
3Univ Med Cntr Freiburg, Freiburgh, Germany.

Meeting: 2016 American Transplant Congress

Abstract number: 480

Keywords: Bone marrow transplantation, Graft-versus-host-disease, Mice, T cells

Session Information

Date: Tuesday, June 14, 2016

Session Name: Concurrent Session: Bone Marrow Transplantation and Chimerism: Animal Models

Session Time: 4:30pm-6:00pm

 Presentation Time: 5:30pm-5:42pm

Location: Room 313

Related Abstracts
  • Recipient IL-33 Promotes Type 1 Alloimmunity and Lethal Acute GVHD Following alloHCT
  • IL-33 Expands ST2+ Regulatory T Cells Promoting Allograft Survival Directly and Indirectly through Actions on Myeloid Dendritic Cells

Background: During allogeneic hematopoietic cell transplantation (alloHCT), non-hematopoietic cell IL-33 is augmented and released by recipient conditioning to promote Type 1 alloimmunity and lethal acute graft-versus-host disease (GVHD). Yet, IL-33 is highly pleiotropic and exhibits potent immunoregulatory properties in the absence of coincident pro-inflammatory stimuli. We tested if administration of IL-33 before alloHCT or "peri-alloHCT IL-33" could protect against development of GVHD by augmenting IL-33-associated regulatory mechanisms.

Methods: For GVHD studies, recipient mice received repeated injections of recombinant IL-33 before total body irradiation (TBI) and alloHCT (bone marrow +/- T cells). Survival, clinical score, and weight were monitored. Changes in immune cell compartments were assessed by flow cytometry and the capacity of regulatory populations to suppress T cell proliferation was verified ex vivo. In related GVHD studies, recipient Treg were depleted from Foxp3-diphtheria toxin receptor (Foxp3DTR) mice by delivering DT concurrently with IL-33 administration.

Results: IL-33 administration doubled recipient regulatory T cells (Treg) and increased suppressive myeloid cells, both of which persist following TBI. Importantly, peri-alloHCT delivery of IL-33 resulted in protection against lethal acute GVHD in the majority of recipients. ST2 expression is not exclusive to Treg and IL-33 expands innate immune cells with regulatory or reparative properties. However, selective depletion of recipient Foxp3+ cells concurrent with peri-alloHCT IL-33 administration accelerated acute GVHD lethality. IL-33-expanded recipient Treg were required for protection from GVHD by controlling macrophage activation and preventing accumulation of CD4+ and CD8+ effector T cells in GVHD target tissue

Conclusions: We demonstrate a protective capacity for peri-alloHCT administration of IL-33 and IL-33-responsive Treg in mouse models of acute GVHD. These findings provide strong support for the concept that the immunoregulatory relationship between IL-33 and Treg can be harnessed therapeutically to prevent GVHD after alloHCT for treatment of malignancy or induction of solid organ transplantation tolerance.

CITATION INFORMATION: Matta B, Reichenbach D, Zhang X, Koehn B, Mathews L, Feser C, Smith M, Liu Q, Zeiser R, Blazar B, Turnquist H. Administration of IL-33 Before Allogeneic Stem Cell Transplantation Expands Recipient Treg That Prevent Graft- vs. Host Disease. Am J Transplant. 2016;16 (suppl 3).

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To cite this abstract in AMA style:

Matta B, Reichenbach D, Zhang X, Koehn B, Mathews L, Feser C, Smith M, Liu Q, Zeiser R, Blazar B, Turnquist H. Administration of IL-33 Before Allogeneic Stem Cell Transplantation Expands Recipient Treg That Prevent Graft- vs. Host Disease. [abstract]. Am J Transplant. 2016; 16 (suppl 3). https://atcmeetingabstracts.com/abstract/administration-of-il-33-before-allogeneic-stem-cell-transplantation-expands-recipient-treg-that-prevent-graft-vs-host-disease/. Accessed January 25, 2021.

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