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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.

journal of immunology research

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

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

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