Volume 130, Issue 1

Cover Figure: Impressive role for ADAMTS13 in vascular repair after ischemic stroke.
See the article by Xu et al.

WASHINGTON, July 6, 2017 – Welcome to “This Week in Blood,” a weekly snapshot of the hottest studies from each week’s issue of Blood, the official journal of the American Society of Hematology (ASH), hand-picked by Blood Editor-in-Chief Bob Löwenberg, MD, PhD, and Deputy Editor Nancy Berliner, MD.

ADAMTS13 controls vascular remodeling by modifying VWF reactivity during stroke recovery
In this plenary paper, Xu et al describe a new function for the metalloprotease ADAMTS13 in blood vessel formation after brain ischemia. Using multiple approaches, they demonstrate an impressive role of ADAMTS13 in neovascularization and vascular repair in mice after ischemic stroke.

Polycomb repressive complexes in hematological malignancies
This comprehensive Blood Spotlight from an author who has shaped the field for years focuses on Polycomb repressive complexes (PRCs) in hematological malignancies and provides a succinct overview of the actions of PRC proteins in normal and malignant hematopoiesis.

Low expression of hexokinase-2 is associated with false-negative FDG–positron emission tomography in multiple myeloma
Rasche and colleagues provide the first evidence of the biological basis underlying the occurrence of false-negative scans with use of [18F]fluorodeoxyglucose (FDG) positron emission tomography/computed tomography in patients with newly diagnosed transplant-eligible multiple myeloma.

Reversion of anergy signatures in clonal CD21low B cells of mixed cryoglobulinemia after clearance of HCV viremia
The phenotype of hepatitis C–related mixed cryoglobulinemia B cells has been previously demonstrated to reflect hypoproliferation in response to stimulation through the B-cell receptor or toll-like-receptor 9, ie, an apparent condition of “anergy.” Del Padre and colleagues evaluate the impact of eliminating chronic antigen exposure on B-cell exhaustion in the human therapeutic setting of antiviral therapy for chronic hepatitis C virus infection complicated by mixed cryoglobulinemia.

Pharmacological targeting of plasmin prevents lethality in a murine model of macrophage activation syndrome
Macrophage activation syndrome is a life-threatening complication characterized by a supraphysiological elevation of cytokines, increase in inflammation, multiorgan dysfunction, and death. Shimazu et al report that cytokine release and activation are mediated through a previously unrecognized LR9/plasmin/MMP9 axis.

Smad1/5 is required for erythropoietin-mediated suppression of hepcidin in mice
How do patients with anemias characterized by ineffective erythropoiesis develop systemic iron overload in the absence of blood transfusions? Wang and colleagues show that Smad1 and Smad5 act cooperatively to increase hepatic hepcidin expression in response to iron-mediated bone morphogenetic signaling. They provide evidence that erythroferrone produced by bone marrow progenitors may suppress hepatic hepcidin expression by inhibiting these same factors.

Donor-engrafted CHIP is common among stem cell transplant recipients with unexplained cytopenias
Gibson et al provide provocative information suggesting that use of otherwise normal stem cell donors with clonal hematopoiesis of indeterminate potential (CHIP) results in impaired hematopoietic recovery after allogeneic hematopoietic cell transplantation.


This week's complete table of contents

Why Submit to Blood?



Blood (, the most cited peer-reviewed publication in the field of hematology, is available weekly in print and online. Blood is the official journal of the American Society of Hematology (ASH) (, the world’s largest professional society concerned with the causes and treatment of blood disorders.

ASH’s mission is to further the understanding, diagnosis, treatment, and prevention of disorders affecting blood, bone marrow, and the immunologic, hemostatic, and vascular systems by promoting research, clinical care, education, training, and advocacy in hematology.

blood® is a registered trademark of the American Society of Hematology.