062 Blockade of CD122 particularly on skin memory T cells suppresses mucocutaneous graft-versus-host disease

Antigen-stimulated naïve T cells differentiate into effector and memory cells, of which resident (TRM) reside permanently in organ tissues. Involvement TRM has been indicated pathological conditions various skin diseases. CD122, is the β chain subunit interleukin (IL)-2 IL-15 receptors, expressed on immune including cells. To investigate whether CD122 signaling CD8+ mediates development mucocutaneous graft-versus-host disease (GVHD), we used a genetically modified mouse expressing membrane-bound form chicken ovalbumin (OVA) under control keratin 14 promoter, develops GVHD-like erosive resulting sclerodermatous after transfer OVA-specific cell-receptor-transgenic OT-I When mice with GVHD were treated an anti-CD122 blocking antibody, acute/chronic our murine model was suppressed via reduction autoaggressive CD122. Moreover, blockade even establishment acute GVHD, inhibited chronic scleroderma epidermal dermal as compared to non-blockade (the median thickness, 203 vs 165 μm, p < 0.05 by Mann-Whitney U test). The suppression might be mediated through interferon (IFN)-γ produced since it reported that IFN-γ stimulates macrophages keratinocytes produce tumor growth factor-β GVHD. Skin CD8+T mediate may effective treatment strategy for