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    Antibodies to the transferrin receptor (TfR) are used to transport therapeutic molecules across the blood-brain barrier. Bien-Ly et al. demonstrate that high-affinity antibodies to TfR trigger internalization and lysosomal degradation of the receptor, impairing the passage of molecules into the brain. These findings help explain the proven superiority of low-affinity anti-TfR antibodies. Image depicts brain endothelial cell nuclei (green) with high-affinity anti-TfR antibodies localizing with the lysosomal marker LAMP1 (red). Art by Lewis Long (
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ISSN 0022-1007
EISSN 1540-9538
In this Issue

Brief Definitive Report

Erythropoietin suppresses non-erythroid cell fate options to induce an erythroid lineage bias at all lineage bifurcations between HSCs and committed erythroid progenitors.

The antiviral drug ganciclovir inhibits microglial proliferation and protects against disease in mice with experimental autoimmunity encephalomyelitis.

The transcription factor Gata3 is required for the generation of group 3 innate lymphoid cells (ILC3) that protect mucosal surfaces.

Hematopoietic stem cells expressing intermediate levels of Kit have superior repopulation capacity after transplantation compared with those expressing high levels of Kit.


c-Kitlo HSCs exhibit enhanced self-renewal and long-term reconstitution potential and give rise to c-Kithi HSCs that have a megakaryocytic bias.

High-affinity transferrin receptor (TfR) bispecific antibodies facilitate trafficking of TfR to lysosomes and induce TfR degradation to decrease the ability of TfR to mediate BBB transcytosis.

Quiescence acts as a safeguard mechanism to ensure survival of the HSC pool during chronic IFN-1 exposure

Reduced expression of bone morphogenetic protein receptor 2 subverts a stress granule response, heightens GM-CSF mRNA translation, and increases inflammatory cell recruitment to exacerbate pulmonary arterial hypertension.

DHA diols produced by Müller cells suppress Notch activation in endothelial cells, thereby promoting retinal angiogenesis.

Blockade of CD28 signals results in the up-regulation of 2B4 on primary CD8+ effectors and plays a critical role in controlling antigen-specific CD8+ T cell responses.

The deubiquitinase USP21 targets RIG-I for deubiquitination, thus dampening interferon production and activation of IFN-responsive genes in response to RNA viruses.

CD73 expression is induced in response to TCR ligation and identifies a population of thymocytes that are committed to the γδ T cell fate.

Memory CD8+ T cells require stronger TCR stimulation than naive cells to enter cell cycle due to reduced Zap70 activation and increased levels of protein tyrosine phosphatases.

Human L chain repertoire includes editor L chains that appear to regulate anti-DNA B cells and shape the B cell repertoire.

Monovalent engagement can trigger BCR signal transduction, and fine-tuning of BCR-ligand recognition can lead to B cell nonresponsiveness, activation, or inhibition.


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