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    Cover Image

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    Dal-Secco et al. show that CCR2+ inflammatory monocytes accumulate around the site of sterile injury, where they switch to CX3CR1+ alternative monocytes and promote tissue repair. The cover image depicts alternative monocytes (blue) entering the injury via blood vessels (orange) and curbing inflammation (yellow) to promote tissue repair. Artwork by Rachel Urkowitz (
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ISSN 0022-1007
EISSN 1540-9538
In this Issue



Mantovani and Allavena provide a comprehensive review on the effects of conventional anticancer therapies on tumor-associated macrophages.

Brief Definitive Report

In response to sterile liver injury, CCR2hiCX3CR1low inflammatory monocytes infiltrate the liver and form a ringlike structure around the injury site. The cells then transition into CCR2lowCX3CR1hi alternative monocytes that enter the injury site; this phenotypic transition was required for optimal repair.

Shade et al. demonstrate the requirement for IgE glycosylation in allergic reactions.

Gao et al. report that genetic or pharmacological blockade of CD95 ligand prevents infiltration of peripheral myeloid cells and thereby averts toxin-induced neurodegeneration in mice.


Lampron et al. use a cuprizone mouse model of demyelination/remyelination to show that in CX3CR1-deficient mice, the clearance of myelin debris by microglia is impaired, affecting the integrity of axon and myelin sheaths.

Dutta et al. show that targeting VACM-1 expression in splenic macrophages impairs extramedullary hematopoiesis, thus reducing inflammation in mouse ischemic heart and atherosclerotic plaques.

Basophils orchestrate eosinophil recruitment during IgE-dependent dermatitis by interacting with inflamed endothelium and producing IL-4. IL-4 in turn induces endothelial VCAM-1 expression, which is required for subsequent eosinophil accumulation.

Tesio at al. identify a novel pathway controlled by the tumor suppressor and deubiquitinase cylindromatosis (CYLD), which is involved in the regulation of hematopoietic stem cell quiescence and repopulation potential.

Crotty and colleagues define the gene targets of BCL6 in primary human follicular T helper cells, revealing its primary role as a gene repressor. BCL6 bound to some loci directly and to others by interacting with AP1 and being recruited to canonical AP1-binding sites.

Matsushita et al. investigated the role of the selenoenzyme glutathione peroxidae 4 (Gpx4) in T cell responses and found that loss of Gpx4 results in an intrinsic T cell developmental defect in the periphery, which leads to a failure to expand and protect from acute viral and parasitic infection.The defects were rescued with dietary supplementation of vitamin E. The Gp4−/− T cells accumulate membrane lipid peroxides and undergo cell death by ferroptosis.

Zhou et al. demonstrate a requirement for the Let-7–Lin28b axis regulating a shift in development between fetal liver and bone marrow B lymphocyte progenitors in the generation of B1 versus B2 B cells. Specifically, the transcription factor Arid3a, induced by Lin28b and a target of Let-7 miRNA, is sufficient to recapitulate fetal B cell development from bone marrow progenitors.

Methot et al. identify a mechanism for cytoplasmic retention of activation-induced deaminase (AID) in cells. Interactions of AID with Hsp90 and eEF1A proteins, both of which stabilize AID, promote sequential folding and retention of functional AID in the cytoplasm. Inhibition of the translation elongation factor eEF1A blocks its interaction with AID, which then accumulates in the nucleus, increasing class switch recombination and the generation of chromosomal translocation byproducts.

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