Our September Issue is out! The cover image shows immunofluorescence staining of nuclei (DAPI, blue), pan-cytokeratin (red), and MHC-II (green) in metastatic lymph nodes in formalin-fixed paraffin-embedded specimens from breast cancer patients.
From Lei et al. (https://doi.org/10.1084/jem.20221847).
Read JEM September Issue: https://rupress.org/jem/issue/220/9
Using antigen-induced arthritis (AIA) model, Zec et al. show that synovial lining macrophages undergo IRF5-dependent activation and produce CXCL1 as a result of
Oral TRM reactivation elicits gingival inflammation. Our July cover shows increased OT-I T cells (white) and pan-leukocytes (red) in buccal mucosa of a novel viral-prime, epitope-pull (VPEP) mouse model, after oral SIIN peptide swabbing. Nuclear and E-Cadherin staining are in green and purple, respectively.
from Stolley et al. (https://doi.org/10.1084/jem.20221853)
Read JEM’s July issue: https://rupress.org/jem/issue/220/7
On our June cover: DNASE1/DNASE1L3 double-knockout (DKO) mice were infected with S. aureus, and their kidneys were examined by immunohistochemistry 72 h later. Sections were stained with DAPI and antibodies against S. aureus (green) and Ly-6G (red). Shown is a low magnification of the entire kidney. From Lacey and colleagues: (https://doi.org/10.1084/jem.20221086).
Read JEM’s June Issue: https://rupress.org/jem/issue/220/6
On our May cover: Qin et al. (https://doi.org/10.1084/jem.20220776) develop a genome-editing tool that combines the versatility of prime editors and unconstrained PAM requirement of SpRY, which is able to rescue retina functionality and restore vision in mice. The cover shows a section of a Pde6bT to C mouse retina immunostained for GFP (green), rhodopsin (red), and nuclei (blue).
Read JEM’s May Issue: https://rupress.org/jem/issue/220/5
On our April cover: Petkova et al. (https://doi.org/10.1084/jem.20220741) identify a new Ptx3-positive immunoregulatory subtype of lymphatic endothelial cells, iLECs, that drive oncogenic PI3K-driven lymphatic malformations. The cover shows a developing dermal venule lesion in a Pik3ca transgenic mouse. The image has been modified by the JEM editorial office.
Read JEM’s April issue: https://rupress.org/jem/issue/220/4
Petkova et al. identify a new Ptx3-positive immune-interacting subtype of lymphatic endothelial cells, iLECs, that drive oncogenic PI3K-driven lymphatic malform
On our March cover: Kaiser et al. show that regulatory T cells infiltrate sites of active viral infection and influence epithelial repair (https://bit.ly/3KMFS2l).
The image shows a lung section of a mouse infected with influenza-labeled (mCherry) virus and labeled Tregs (green) and stained for secreted extracellular matrix proteoglycan Agrin (white). The image has been modified by the JEM editorial office.
Read JEM’s March Issue: https://rupress.org/jem/issue/220/3
Gut microbiota biofilms: From regulatory mechanisms to therapeutic targets.
In this Viewpoint, Andre Buret and Thibault Allain discuss the mechanisms that regulate gut microbiota biofilms integrity and highlight the importance of studying phenotypic biofilm damage, beyond the characterization of relative bacterial abundance. https://rupress.org/jem/article/220/3/e20221743/213820/Gut-microbiota-biofilms-From-regulatory-mechanisms?utm_source=mastodon
Andre Buret and Thibault Allain discuss the mechanisms that regulate gut microbiota biofilms integrity and highlight the importance of studying phenotypic biofi
The animal model for experimental encephalomyelitis, first published 90 yr ago, continues to illuminate mechanisms of disease. The model, initially developed to understand how smallpox triggers neuroinflammation on rare occasions, now moves full circle to its origins.
A Perspective from Lawrence Steinman, Roberto Patarca, and William Haseltine: https://rupress.org/jem/article/220/2/e20221322/213807/Experimental-encephalomyelitis-at-age-90-still?utm_source=mastodon
The animal model for experimental encephalomyelitis, first published 90 yr ago, continues to illuminate mechanisms of disease. The model, initially developed to
Nielsen and Zhang et al. show that well-established, Notch4-induced brain arteriovenous malformations are normalized, following deletion of the Notch signaling
