Skip to Main Content

Advertisement

Skip Nav Destination
Newest Articles
Article
Atsushi Tanaka et al.
How an anomaly in a TCR signaling molecule leads to spontaneous autoimmunity over immunodeficiency is unclear. Qualitative/quantitative reduction of ZAP-70 to a critical range produces autoimmune T cells and impairs Treg function, together eliciting autoimmune arthritis and colitis in mice.
Brief Definitive Report
Gretchen Harms Pritchard et al.
The study identifies a unique role for early T-bet expression in promoting the proliferation of antigen-specific CD8+ T cells following vaccination. Early T-bet expression is necessary for optimal LFA1 expression for appropriate cellular interactions and enables optimal expansion and differentiation of effector and memory CD8+ T cells.
Brief Definitive Report
Corinne M. Nielsen et al.
Nielsen and Zhang et al. show that well-established, Notch4-induced brain arteriovenous malformations are normalized, following deletion of the Notch signaling mediator, Rbpj. Upon complete regression, virtually no AVM relapses in adults, even when the causal factor is reintroduced.
Article
Juan D. Matute et al.
ITLN1, whose expression is regulated by the unfolded protein response, coats a subset of microorganisms, including Akkermansia muciniphila, allows them to thin the inner mucus layer, and increases colitis severity. ITLN1 upregulation in UC may drive similar outcomes.
Brief Definitive Report
Anna Onnis et al.
We report a new mechanism of immune evasion by SARS-CoV-2 based on direct disabling CTLs to form immune synapses through Spike protein binding to ACE2. This mechanism could contribute to the failure of the immune system to control SARS-CoV-2 infection.
Article
Akiko Nakayama et al.
The authors identify a tumor-suppressing angiocrine function of CCL2 which is inhibited by tumor-derived adrenomedullin acting via its receptor on endothelial cells. Disinhibition of endothelial CCL2 results in reduced tumor progression through inhibition of adrenomedullin formation by tumor cells.
Article
Yifan Zhou et al.
Zhou et al. establish murine models of anti-CTLA-4–mediated intestinal irAEs. These reveal common immune signatures and the importance of fecal microbiome dysbiosis as irAE-driving mechanisms, which enable preclinical therapeutic interventions. Key immune features are validated in a cohort of melanoma patients with ICB-associated intestinal irAEs.

Related Articles from Rockefeller University Press

Issue Cover
Current Issue
Volume 219,
Issue 11,
7 November 2022
Reviews & Opinions
Insights
Charles R. Schutt, Sho Yamasaki
ITLN1, whose expression is regulated by the unfolded protein response, coats a subset of microorganisms, including Akkermansia muciniphila, allows them to thin the inner mucus layer, and increases colitis severity. ITLN1 upregulation in UC may drive similar outcomes.
Insights
Gillian Carling et al.
In this important study, Jain et al. find that chronic TREM2 activation by AL002a antibody exacerbates the seeding and spread of pathological tau, enhances the disease-associated microglial signature, and increases neurite dystrophy in 5xFAD mice seeded with Alzheimer’s disease tau.
Insights
Andrew Sandstrom
In this issue of JEM, Jenster et al. investigate how UVB radiation promotes activation of the inflammatory immune sensor NLRP1, and in doing so uncover how NLRP1 recognizes a diverse range of ribotoxic stresses.

Most Read

Advertisement

Tweets by @JExpMed

Special Collections

Special Collections

Our annual Best of JEM series, featuring articles that were of great interest to our readers..

View all collections
Close Modal

or Create an Account

Close Modal
Close Modal