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The Strathprints institutional repository is a digital archive of University of Strathclyde research outputs.

Strathprints serves world leading Open Access research by the University of Strathclyde, including research by the Strathclyde Institute of Pharmacy and Biomedical Sciences (SIPBS), where research centres such as the Industrial Biotechnology Innovation Centre (IBioIC), the Cancer Research UK Formulation Unit, SeaBioTech and the Centre for Biophotonics are based.

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Cutting edge: acute lung allograft rejection is independent of secondary lymphoid organs

Gelman, Andrew E. and Li, Wenjun and Richardson, Steven B. and Zinselmeyer, Bernd H. and Lai, Jiaming and Okazaki, Mikio and Kornfeld, Christopher G. and Kreisel, Friederike H. and Sugimoto, Seiichiro and Tietjens, Jeremy R. and Dempster, J. and Patterson, G. Alexander and Krupnick, Alexander S. and Miller, Mark J. and Kreisel, Daniel (2009) Cutting edge: acute lung allograft rejection is independent of secondary lymphoid organs. Journal of Immunology, 182. pp. 3969-3973. ISSN 0022-1767

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Abstract

It is the prevailing view that adaptive immune responses are initiated in secondary lymphoid organs. Studies using alymphoplastic mice have shown that secondary lymphoid organs are essential to initiate allograft rejection of skin, heart, and small bowel. The high immunogenicity of lungs is well recognized and allograft rejection remains a major contributing factor to poor outcomes after lung transplantation. We show in this study that alloreactive T cells are initially primed within lung allografts and not in secondary lymphoid organs following transplantation. In contrast to other organs, lungs are acutely rejected in the absence of secondary lymphoid organs. Two-photon microscopy revealed that recipient T cells cluster predominantly around lung-resident, donor-derived CD11c+ cells early after engraftment. These findings demonstrate for the first time that alloimmune responses following lung transplantation are initiated in the graft itself and therefore identify a novel, potentially clinically relevant mechanism of lung allograft rejection.