Issue Archive

Developments from studies of cell biology are beginning to offer improved methods for clinical diagnosis, evaluation, and management of graft-versus-host disease (GVHD), especially for measuring severity and response to treatment.

The article by Komanduri et al in this issue of Blood describes immune reconstitution after human leukocyte antigen (HLA)-mismatched cord-blood transplantation. As expected, a profound reconstitution deficiency was observed; a study of some subpopulations could be predictive of the outcome.

In this issue of Blood, Brown and colleagues deliver lentiviral vectors that express human factor IX from the livers of mice.

Newly formed lymphatic capillaries closely associated with malignant tumors have a key role in metastasis, but much remains to be learned about the trigger and mechanisms of lymphangiogenesis. In this issue of Blood, Kilic and colleagues report that CEACAM1, recognized as a possible lymphangiogenic switch, is expressed in newly formed tumor-associated lymphatic capillaries, and that it can trigger reprogramming of microvascular endothelial cells to lymphatic endothelial cells.

In this issue of Blood, Guzman and colleagues describe 2 significant advances in the selective targeting of leukemic progenitor cells. First, they identify a novel agent, TDZD-8, that induces apoptosis of leukemic stem cells (LSCs) with extremely rapid kinetics. Second, they describe the development of an orally bioavailable parthenolide (PTL) analog, DMAPT, that is now heading to phase 1 clinical trial following the preclinical work described in this issue.

Knocking out the immunodominant antigen (Band 3) in a spontaneous model of mouse autoimmune hemolytic anemia demonstrates that full pathology still occurs even in the absence of the normal target of autoantibodies.

In this issue of Blood, Navarro and colleagues report the first molecular evidence for a pTα intracellular adaptor involved in human pre-TCR (T-cell receptor) function.

In this issue of Blood, Yamaguchi and colleagues demonstrated the essential role of the β2-glycoprotein I (β2GPI)/phosphatidylserine complex opsonized by IgG anti-β2GPI antibodies in the proliferation of CD4⁺ T cells in patients with anti-phospholipid syndrome. Their findings provide novel clues for specific targeting therapies in the affected patients.