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CD137 Signaling in Regulatory Dendritic Cells Is Required for Suppressing a Systemic Inflammation in the bm12-Inducible Model of Systemic Lupus Erythematosus

H. Cho1, J. Lee2, B. Kwon3, S. Park1, H. Park1, K. Yoo2, K. Park2, J. Kim3

1Surgery, Ulsan University Hospital, Ulsan, Korea, Republic of, 2Nephrology, Ulsan University Hospital, Ulsan, Korea, Republic of, 3Biomedical Research Center, Ulsan University Hospital, Ulsan, Korea, Republic of

Meeting: 2020 American Transplant Congress

Abstract number: D-373

Keywords: Autoimmunity, Co-stimulation, Graft-versus-host-disease, Immune deviation

Session Information

Session Name: Poster Session D: Tolerance / Immune Deviation

Session Type: Poster Session

Date: Saturday, May 30, 2020

Session Time: 3:15pm-4:00pm

 Presentation Time: 3:30pm-4:00pm

Location: Virtual

*Purpose: Although CD137 is well known as a costimulatory receptor in T cells, limited information is available for its immunoregulatory function. Here, we report that CD137 signaling maintains CD11b+ regulatory dendritic cells (DCs) that can suppress activation of donor TH1 and TH17 CD4+ T cells in systemic erythematosus lupus (SLE)-like chronic graft-versus-host disease

*Methods: Female C57BL/6 (H-2b) mice were purchased from Orient. CD137-/- (H-2b) and B6.C-H2bm12 (H-2bm12) mice were bred at the animal facility of the Biomedical Research Center at University of Ulsan. All of mice were used at 8-10 wks of age. Single-cell suspensions in PBS were prepared from the spleens and lymph nodes of female bm12 mice. The erythrocytes were lysed in RBC lysis buffer (BioLegend), the remaining cells were re-suspended at 8 x 107 cells/0.2 ml in PBS. Chronic GVHD was induced by transfer of 8 x 107 of bm12 cells into the tail vein of female wild-type and CD137-/- mice. Immediately thereafter, 200 μg of anti-CD137 mAb (3E1) or control Ig was intraperitoneally administered. And then we check the flowcytometry, ELISA, RT PCR, and liver and colonic histology.

*Results: Deletion of CD137 in recipient mice shifted the disease phenotype toward acute GVHD, which was caused by activation of donor T cells and subsequent multiple organ. CD137-/- recipients had had characteristic changes associated with acute GVHD: 1) there were defects in differentiation of T follicular helper (TFH) cells, germinal-center B cells, and plasma cells, and in production of anti-DNA IgG1 autoantibody; 2) their splenic DCs showed dysregulated expression of DC-specific transcription factors and proinflammatory genes; and 3) there were strong activation of donor T cells but decreased Treg cells in the CD137-/- recipient spleen. CD11b+ splenic DCs stimulated with anti-CD137 antibody and CpG markedly increased expression of immunomodulatory genes and such regulatory DCs inhibited acute GVHD in CD137-/- recipients. Their suppressive action was mediated through IL-10 that is indispensable for the induction and expansion of peripheral of Treg cells.

*Conclusions: . In conclusion, our study identifies CD137 signaling in DCs as an important braking point to prevent systemic inflammation and this control system may be considered as a therapeutic strategy for a variety of inflammatory and autoimmune diseases.

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To cite this abstract in AMA style:

Cho H, Lee J, Kwon B, Park S, Park H, Yoo K, Park K, Kim J. CD137 Signaling in Regulatory Dendritic Cells Is Required for Suppressing a Systemic Inflammation in the bm12-Inducible Model of Systemic Lupus Erythematosus [abstract]. Am J Transplant. 2020; 20 (suppl 3). https://atcmeetingabstracts.com/abstract/cd137-signaling-in-regulatory-dendritic-cells-is-required-for-suppressing-a-systemic-inflammation-in-the-bm12-inducible-model-of-systemic-lupus-erythematosus/. Accessed May 10, 2025.

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