Effector T cell migration to pancreatic islet allografts is dependent on donor antigen recognition and not Gai chemokine signaling. (TRAN1P.945)

• DOI: 10.4049/jimmunol.194.supp.140.27
• Publication Date: 2023-01-01T09:55:32Z
• Authors: Qianqian Zhang; Hehua Dai; Qiang Zeng; Amanda Williams; Martin Oberbarnsc...; Fadi Lakkis
• Keywords: 0303 health sciences; 03 medical and health sciences

Abstract Host effector T cell graft infiltration is a key step in the pathogenesis of both acute and chronic rejection. Recent data indicate migration into primary vascularized organ transplants such as heart kidney driven by donor antigen recognition, not via Gai-coupled chemokine receptor signaling. Whether it true for neovascularized pancreatic islet allografts unknown. We co-transferred pertussis toxin (Ptx)-treated untreated TCR-tg (OT-1) cells B6 recipients 7-10 days after transplanting B6-Act-OVA or grafts under capsule. Ptx irreversibly blocks Gai-dependent Grafts were imaged 20-24 hours transfer two-photon intravital microscopy. observed heavily infiltrated with OT-1 irrespective pre-treatment (453.7+/-170.0 vs. 632.8+/-221.1 per imaging volume, n = 10, p 0.0522 ), while grafts, which lack cognate recognized cells, free infiltrate (<5 7). These results that, similar to transplants, allograft host antigen, Gai The paradigm antigen-driven therefore generalizable antigens are abundantly expressed on endothelium, cellular whereby endothelium origin.