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Journal of Immunology Research
Volume 2018, Article ID 1605341, 13 pages
https://doi.org/10.1155/2018/1605341
Research Article

Anti-IL-22 Antibody Attenuates Acute Graft-versus-Host Disease via Increasing Foxp3+ T Cell through Modulation of CD11b+ Cell Function

1Department of Liver Surgery, First Affiliated Hospital of Nanjing Medical University, Key Laboratory of Living Donor Liver Transplantation, National Health and Family Planning Commission, Nanjing, Jiangsu Province, China
2Department of General Surgery, Changzhou No. 2 People’s Hospital Affiliated to Nanjing Medical University, Changzhou City, Jiangsu Province, China

Correspondence should be addressed to Ling Lu; nc.ude.umjN@100gnilvl and Xuehao Wang; nc.ude.umjn@hxgnaw

Received 25 February 2018; Revised 20 June 2018; Accepted 28 June 2018; Published 7 August 2018

Academic Editor: Martin Holland

Copyright © 2018 Jianbo Wu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Transfer of splenocytes isolated from B6 mice into normal B6D2F1 mice induces acute graft-versus-host disease (aGVHD), resulting in the expansion of donor cytotoxic T lymphocytes that eliminate recipient B cells. The cytokine IL-22, secreted by Th1 cells, Th17 cells, and innate immune cells, is structurally related to IL-10. To investigate the association between IL-22 and aGVHD, an anti-mouse IL-22 antibody (IL-22Ab) was used to ablate IL-22 activity in a mouse aGVHD model. Administration of IL-22Ab significantly reduced the progression of aGVHD in B6D2F1 recipients of B6 grafts. IL-22Ab treatment also decreased the percentage of interferon-γ+ and tumor necrosis factor-α+ T cells but increased the number of forkhead box p3+ regulatory T cells (Tregs). In the presence of Tregs and donor CD11b+ cells, IL-22Ab protected against aGVHD. In vitro Treg induction was more efficient when CD4+CD25 T cells differentiated in the presence of CD11b+ cells obtained from IL-22Ab-treated GVHD mice, compared with cocultured untreated control cells. Finally, IL-22Ab modulated the expression of cytokines and costimulatory molecules in CD11b+ cells in aGVHD mice. We therefore conclude that IL-22Ab administration represents a viable approach for treating aGVHD.