Naïve CD8 T cell subsets marked by IL-18Rα, CD73, and CXCR3 exhibit superior persistence and enhance effector and memory responses, boosting immune protection.
Journal of Experimental Medicine
Rockefeller University Press · Immunology & Inflammation · ISSN 0022-1007, 1540-9538
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CAMKV kinase, previously thought inactive, is essential for neuroblastoma growth and correlates with poor patient outcomes, revealing a new therapeutic target.
UA-30 delays systemic aging and improves muscle function in naturally aged mice by inhibiting RalA signaling, reducing fibrosis, and extending lifespan.
Alox15 is essential for M2 macrophages to trap and kill helminths by restraining glycolysis, despite normal M2 marker expression, revealing a metabolic control mechanism.
C3 and CD47 collaboratively eliminate supernumerary synapses in spinal circuits, ensuring proper motor development in mammals.
Vps4B orchestrates caspase-1 recruitment and activation at the ASC speck, enabling continuous inflammasome signaling essential for host defense.
Borrelia burgdorferi causes a "leaky gut" syndrome in mice and humans, disrupting gut barrier function and immune responses during Lyme disease.
Silencing TNFR1 on tumor cells reduces immune escape by decreasing MDSC recruitment, impairing tumor growth in immunocompetent hosts.
Long-lived naive CD8 T cells acquire tonic TCR signaling that enhances their differentiation into more effective effector cells.
Homozygous loss-of-function RORγT variants cause severe T cell deficiencies and susceptibility to mycobacterial and candidiasis infections in humans.
Autoantibodies neutralizing type I IFNs cause approximately 5% of adult herpes simplex encephalitis cases, mainly targeting IFN-ω.
Vagal neuroimmune circuits play a crucial role in regulating inflammation and immunity, with the vagus nerve integrating inflammatory signals to influence immune responses in health and disease.
Qdenga vaccine induces serotype-skewed antibody responses with only 8% of DENV-naive individuals developing balanced tetravalent immunity.
Loss of Helios in Tregs causes dysfunctional effector Treg differentiation, leading to adipose tissue destruction and systemic metabolic disease in mice.
GABPA transcription factor, activated by IKKε phosphorylation, enhances STING expression and amplifies antiviral and inflammatory responses in macrophages.
Upper respiratory tract CD8+ tissue-resident memory T cells alone can prevent viral transmission, with URT TRM activation sufficient for protection in mice.
IL-17 activates a tPA-LRP1 pathway that protects the renal epithelium during systemic candidiasis, highlighting a novel organ-preserving immune mechanism.
Antibody-mediated enhancement of germinal center and plasma cell responses depends on Fc gamma receptor but not complement receptors, while affinity threshold reduction is receptor-independent.
Broadening CSP regions targeted in malaria vaccines enhances immune responses and protection, with a 2-fold increase in antibody diversity and efficacy.
SorLA controls B cell receptor trafficking and immune responses, with its deletion reducing plasma cells and humoral immunity in vivo.
tPA protects against kidney damage in invasive Candida albicans infections by reducing renal tubular epithelial cell apoptosis, with a significant role in preserving kidney integrity.
PML::RARA fusion enhances hematopoietic progenitor immortalization by promoting sumoylation of repressive complexes, with UBC9 recruitment being essential for transformation.
Long-term neural implant instability stems from erosion of cell lineage programs, disrupting tissue function and leading to reactive gliosis and signal loss.
CD1d deletion or targeting reduces breast tumor growth and improves anti-PD-1 therapy by remodeling tumor-infiltrating myeloid cells, increasing inflammatory monocytes.
TL1A-blocking antibodies show promise as a highly effective therapy for IBD, with early phase 2 studies reporting some of the highest response rates in UC and CD.
LAG3+CD8+ tumor-reactive T cells differentiate into terminally exhausted and long-lived memory cells, with the latter essential for sustained anti-tumor immunity.
Tethered orthogonal IL-2 engineered into Tregs enhances their survival and prevents autoimmune diabetes in mice by enabling self-sustaining autocrine signaling.
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