S100A9 separates GVHD from GVL

Kim S, Lim S, Kim B, et al. S100A9 Up-Regulated by IFNGR Signaling Blockade Functions as a Novel GVHD Suppressor Without Compromising GVL in Mice. Blood. 2022; (doi: 10.1182/blood.2021012687).

Researchers are learning more about how S100A9 protects patients from graft-versus-host disease (GVHD) after stem cell transplantation. They now know the downstream molecule is upregulated when interferon-gamma receptor (IFNGR) signaling is blocked in T cells and that inhibition of graft-versus-host disease (GVHD) is the result. Importantly, antitumor function is preserved even as this process occurs. In mice, administration of recombinant S100A9 proteins or up-regulation of S100A9 by anti-IFNGRα antibodies curtailed GVHD in subjects. Rodents that received the proteins also lived longer overall than control mice. In vivo introduction of anti-human IFNGRα antibody improved GVHD in a mouse model of xenogeneic human peripheral blood mononuclear cell transplantation.

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Tags: patient care, GVHD, transplantation, Treatment, Cellular therapy, Research, Graft versus host disease, grafts, graft-versus-host disease, graft-vs-host disease, T cells, T cell, stem cell transplant

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