Issues

Microcontact printing can be used to mimic spatially limiting Ag presentation.

High synapse propensity of human memory CD8 T cells prevents naive cell recruitment.

Part of the juxtamembrane of BTN3A1 proteins forms a coiled-coil dimer.

The coiled-coil dimer is critical for BTN3A1 stimulation of Vγ2Vδ2 T cells.

B30.2 domains of BTN3A1 proteins also dimerize through a short coiled-coil region.

YY1-deficient NKT cells display cell-intrinsic developmental and functional defects.

YY1-deficient NKT cells maintain wild-type levels of PLZF expression.

YY1 and PLZF proteins associate with one another.

The CD27 pathway on CD4⁺ T cells plays a role in driving skin autoimmunity.

CD27 signaling promotes survival by suppressing cell-extrinsic apoptosis.

Seminal fluid primes Treg cells to elicit tolerance of male alloantigens.

Neuropilin-1⁺ Tregs of likely thymic origin are prevalent amongst responding T cells.

Neuropilin-1⁺ Tregs exhibit Foxp3 TSDR demethylation after seminal fluid contact.

The transcriptional regulator Id2 is highly expressed in aTregs.

Id2 is critical for the survival of aTregs.

Id2 is essential for the function of aTregs in preventing systemic inflammation.

BACE1 is expressed in CD4⁺ T cells and regulates signaling events during activation.

BACE1-deficient T cells show reduced IL-17A expression in vitro.

BACE1^−/− Th17 cells have impaired pathogenicity in EAE.

Three signals are required to trigger NK cell proliferation.

4-1BBL fine-tunes NK cell proliferation but not NK cell cytolytic activity.

REs critical for Foxn1 expression are in the first intron of Foxn1.

These elements are necessary for Foxn1 expression in TECs.

These elements are not required for Foxn1 expression in the skin.

Recombinant adeno-associated virus expresses low and sustained levels of IFN-α.

AAV–IFN-α exerts a potent therapeutic effect and low toxicity in an EAE animal model.

KIRs and NK cytotoxicity correlate with HIV control upon IFN-α immunotherapy.

NK activity–associated genes correlate with HIV DNA decline upon IFN-α immunotherapy.

A gene signature identifies subjects with no ISG modulation upon IFN-α immunotherapy.

TRAIL binding to TRAIL receptor R1 and R2 contributes to CD4 death during HIV infection.

Blocking TRAILshort, a TRAIL antagonist, increases death of HIV-infected and uninfected cells.

Homeostatic production of TRAILshort may protect cells from HIV-induced cell death.

Immunoparalysis phase of sepsis is characterized by increased tumor progression.

Effector PD-1^hi CD8 TILs are reduced in frequency/function in sepsis survivors.

Checkpoint blockade therapy has a diminished window of efficacy in sepsis survivors.

MSU crystals and alum rapidly activate GSDMD.

GSDMD is dispensable for MSU crystal– and alum-induced IL-1β release and cell death.

Cathepsins, caspases, and MLKL are not required for MSU crystal–induced cell killing.

Automated machine learning approach to identify vaccine-induced immune signatures.

Analysis of multidimensional clinical data collected across multiple cohorts.

Increasing predictive performance of models by using heterogenous clinical data.

Microfluidics provides precision for manipulating cell–cell interactions.

Complex mitochondrial movement occurs during initial T cell:APC synapse formation.

Mitochondrial positioning is a strong predictor of calcium response.