IL-6 receptor (IL-6R) blockade with tocilizumab during allogeneic HSCT induces type I interferon-driven transcriptional programs in CD4+ T cells and CD14+ monocytes.
IL-6R inhibition selectively enhances the expansion of cytolytic, eomesodermin-positive (Eomes+) CD4+ T cells with regulatory and antitumor properties.
Genetic disruption of IL-6 signaling in donor T cells attenuates Th1 and Th17 differentiation, improving graft-versus-tumor effects and reducing graft-versus-host disease (GVHD).
These findings provide mechanistic insight into how IL-6R inhibition modifies immune reconstitution post-HSCT and support its therapeutic potential to enhance immunotherapy efficacy.
