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Circulating dsDNA, endothelial injury, and complement activation in thrombotic microangiopathy and GVHD
Author(s) -
Nicholas J. Gloude,
Pooja Khandelwal,
Nathan Luebbering,
Dana T. Lounder,
Sonata Jodele,
Matthew N. Alder,
Adam Lane,
Alyss Wilkey,
Kelly E. Lake,
Bridget Litts,
Stella M. Davies
Publication year - 2017
Publication title -
blood
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.515
H-Index - 465
eISSN - 1528-0020
pISSN - 0006-4971
DOI - 10.1182/blood-2017-05-782870
Subject(s) - thrombotic microangiopathy , medicine , complement system , immunology , microangiopathy , antibody , disease , endocrinology , diabetes mellitus
Key Points dsDNA production peaks 14 days after HSCT, likely a result of IL-8–driven neutrophil recovery. dsDNA production may serve as a mechanistic link between endothelial injury, TA-TMA, and GVHD.

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