Newest Articles
- Early T-bet expression specifies a Tfh cell subset
The mechanisms underlying the differentiation of T follicular helper (Tfh) cell subsets are poorly understood. Here, Fang et al. show that the NKG2Dhigh Tfh cells in germinal centers with a history of T-bet expression represent the IFN-γ–producing Tfh subset.
- USP38 stabilizes JunB in TCR signaling
Although usp38 has recently been reported to be in a chromosome locus associated with human asthma in a GWAS study, its potential pathological role remains unknown. Chen et al. now demonstrate that usp38 is essential for asthmatic pathogenesis. USP38 is induced by TCR signaling and in turn promotes JunB stabilization to specifically regulate Th2 cell differentiation.
- Retinoids suppress MYB in adenoid cystic carcinoma
Adenoid cystic carcinoma (ACC) is a salivary gland malignancy that has no effective therapy and is caused by translocations involving MYB. A zebrafish chemical genetic screen identifies the retinoic acid class of compounds as potential MYB-inhibitory agents. Preclinical ACC mouse xenotransplantation models confirm the in vivo efficacy of retinoic acid, which represents a potential therapy for ACC.
- Dual origin of macrophages in lung tumors
Loyher et al. demonstrate that lung tumors are densely colonized by macrophages of various ontogenies. These distinct developmental origins dictate tumor-associated macrophages relative anatomical distributions, functions and responses to anti-cancer therapies.
- Origin of ECs during tissue regeneration
Employing a broad array of genetic lineage–tracing protocols including parabiotic pairs, Singhal et al. reveal that the fitness of liver endothelial cells (ECs) determines whether resident ECs or bone marrow–derived mononuclear cells will be adopted for vascular regeneration.
- Piezo1 and Gq/G11 promote endothelial inflammation
Atherosclerosis preferentially develops in areas of disturbed flow. Albarrán-Juárez et al. provide evidence that this depends on at least two different endothelial mechanosignaling pathways, a flow direction-independent pathway involving Piezo1 and Gq/G11, as well as integrin signaling, which is only initiated in response to disturbed flow.
- aPIK3CD expands innate B cells but limits function
B cell–intrinsic expression of activated PIK3CD (aPIK3CD) restricts immature BM B cell development while promoting the expansion of MZ and B1a B cells via enhanced survival. aPIK3CD is counter-productive during both T cell–independent and –dependent responses, limiting antigen-specific antibodies and class-switch recombination.












In this issue of JEM, Singhal et al. explore the cellular mechanisms involved in endothelial cell regeneration in the liver. Using a combination of myeloablative and nonmyeloablative approaches, the authors found that repair of the endothelium is mediated by endothelial cells themselves, but when injured, endothelial cells enlist myeloid counterparts that aid in vascular repair.