Issue Archive

In this issue of Blood, Das et al assign a very novel and unanticipated function to plasminogen by showing that it is an enhancer of the phagocytic function of macrophages.¹ 

In this issue of Blood, Jitschin et al identify increased numbers of myeloid-derived suppressor cells (MDSCs) in untreated patients with chronic lymphocytic leukemia (CLL) suppressing T cells and inducing regulatory T cells (T_regs), resulting in impaired immune responses.¹ 

In this issue of Blood, Lu et al describe the cooperation between an orally bioavailable mouse double minute 2 (MDM2) antagonist (RG7112) and the pegylated interferon α (Peg-IFNα 2a) to target JAK2V617F hematopoietic progenitors and stem cells. Their work provides a rationale for the treatment of patients suffering from myeloproliferative neoplasms (MPNs).¹ 

In this issue of Blood, Keerthivasan et al have identified that the deletion of mDia1, a chromosome 5q gene, contributes to myelodysplastic syndromes (MDSs) by increasing innate immune signaling in granulocytes.¹ 

In this issue of Blood, Koupenova and colleagues report that platelets express functional TOLL-like receptor 7 (TLR7) and contribute to host survival during viral infection.¹  Through a series of experiments utilizing mice deficient for TLR7 together with adoptive transfer of wild-type platelets, Koupenova et al¹  demonstrate that platelets specifically respond to viral analogs and intact virus, leading to platelet activation and binding to various leukocyte subsets. Perhaps most importantly, this platelet activation appears absolutely essential for host survival during infection with some viral pathogens such as encephalomyocarditis virus (EMCV).

In this issue of Blood, Liu et al gain an understanding of phenotypic variability in hemoglobinopathies.¹  They find that mutations in Krüppel-like factor-1 (KLF1) are significantly more prevalent in patients with β-thalassemia than previously recognized and correlate with a milder phenotype. This supports the emerging concept that monoallelic KLF1 mutations can play a modulatory role in hemoglobinopathies.

In this issue of Blood, Hazenberg and Spits provide a detailed overview of human innate lymphoid cell (ILC) subsets and their development and distribution throughout the human body, discussing these cells in the context of human disease. In the same issue, Munneke et al for the first time link ILCs to human hematopoietic malignancies by identifying a clear correlation between the presence of activated ILCs after induction chemotherapy and the absence of acute graft-versus-host disease (GVHD) development following subsequent hematopoietic stem cell transplantation (HSCT).^1,2 

In this edition of Blood, Bertaina et al report 3-year survival exceeding 90% by using haploidentical αβ⁺CD3⁺/CD19⁺-depleted allogeneic transplantation for children with nonmalignant disorders.¹