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Eric Vivier and colleagues discuss recent publications demonstrating that T reg cell restriction of IL-2 availability regulates NK cell function.

Brief Definitive Report

Ubiquitination of MHCII molecules on dendritic cells is essential for the development of natural regulatory T cells

Loss of TRAF3 results in reduced TCR signaling and defective up-regulation of T-bet and CD122 in iNKT cells that impairs their proliferation and survival.

RB family genes control T cell production and promote thymic involution through reducing Foxn1 expression in thymic epithelial cells.

Chemokine receptor CXCR4 promotes B cell localization to CXCL12+ perilymphatic zones and egress from Peyer’s patches.

A new polymorphism near the IL28B locus negatively affects induction of IL28B and exhibits strong predictive value for HCV treatment response and spontaneous resolution.

Retinoic acid attenuates colitis and is associated with increased IL-22 production from γδ T cells and innate lymphoid cells and enhanced antimicrobial peptide expression.

Transfer of FAP-reactive T cells into mice bearing a variety of subcutaneous tumors mediated limited antitumor effects and induced significant cachexia and lethal bone toxicities


Ablation of stromal cells expressing fibroblast activation protein-α (FAP) results in cachexia and anemia, and loss of these cells is seen in transplantable tumor models.

Pancreatic T reg cells control the availability of CD4+ T cell–secreted IL-2 to limit NK cell function.

IL-2–dependent adaptive-innate lymphocyte cross talk tunes NK cell reactivity and is limited by T reg cells.

T reg cells restrain IL-2–mediated expansion of immature CD127+ NK cells.

The transcription factor Foxo1 is required for the differentiation of memory CD8+ T cells, and its absence hinders clearance of secondary infections.

Dexamethasone suppresses ER stress in inflammatory bowel disease by promoting correct protein folding and ER-associated degradation.

PLA2G2D ameliorates skin inflammation through mobilizing pro-resolving lipid mediators.

Mutating anti–HIV-1 broadly neutralizing antibodies increases their breadth and reduces pathways for viral escape through mutation.

CD172a+ cells producing IL-1β and TNF are increased in inflamed tissues in Crohn’s disease and can be targeted by CD47 fusion protein.

Group B Streptococcus invades human amniotic epithelial cells using a hemolytic pigment.

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