Treg engage lymphotoxin beta receptor for afferent lymphatic transendothelial migration

C. Colin Brinkman, Daiki Iwami, Molly K. Hritzo, Yanbao Xiong, Sarwat Ahmad, Thomas Simon, Keli L. Hippen, Bruce R. Blazar and Jonathan S. Bromberg ()
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C. Colin Brinkman: Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine
Daiki Iwami: Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine
Molly K. Hritzo: University of Maryland School of Medicine
Yanbao Xiong: Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine
Sarwat Ahmad: Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine
Thomas Simon: Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine
Keli L. Hippen: University of Minnesota Cancer Center
Bruce R. Blazar: University of Minnesota Cancer Center
Jonathan S. Bromberg: Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine

Nature Communications, 2016, vol. 7, issue 1, 1-16

Abstract: Abstract Regulatory T cells (Tregs) are essential to suppress unwanted immunity or inflammation. After islet allo-transplant Tregs must migrate from blood to allograft, then via afferent lymphatics to draining LN to protect allografts. Here we show that Tregs but not non-Treg T cells use lymphotoxin (LT) during migration from allograft to draining LN, and that LT deficiency or blockade prevents normal migration and allograft protection. Treg LTαβ rapidly modulates cytoskeletal and membrane structure of lymphatic endothelial cells; dependent on VCAM-1 and non-canonical NFκB signalling via LTβR. These results demonstrate a form of T-cell migration used only by Treg in tissues that serves an important role in their suppressive function and is a unique therapeutic focus for modulating suppression.

Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12021

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DOI: 10.1038/ncomms12021

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