Issues

FcεRI-mediated mast cell function is susceptible to isoprenylation inhibitors.

K-Ras is a critical component of FcεRI-mediated mast cell activation.

Targeting isoprenylation can suppress allergic inflammation in vivo.

NK cells from HCMV⁺ individuals have elevated levels of glycolytic metabolites.

NK cells from HCMV⁺ individuals exhibit very high levels of deoxyribonucleotides.

Adaptive NK cells exhibit more robust mTORC1 activation in response to activation.

CD103 restrains Treg migration in inflamed skin when E-cadherin is upregulated.

CD103 supports interactions of Tregs with CD11c-expressing cells in inflamed skin.

CD103 inhibition increases inflammation in contact hypersensitivity.

Distinct glutamine inhibition strategies cause unique changes to CD8 T cell function.

T cell metabolism compensates according to how glutamine metabolism is targeted.

Timing and strategy for use of glutamine-targeting agents modify T cell outcomes.

pDCs cooperate with B cells through the production of IFN-I and CXCL10.

pDCs enhance the T-independent B response through a p38 MAPK–STAT1 axis.

pDCs enhance TLR-stimulated autoantibody production in FO B and MZ B cells.

miR-308 targets Tab2 to negatively regulate the immune response.

Relish binds the promoter and activates the expression of miR-308.

The Relish–miR-308–Tab2 axis is critical for immune homeostasis in the Drosophila Imd pathway.

M. tuberculosis induces RARE genes by human monocytes.

M. tuberculosis metabolizes serum components and activates RAR pathway.

BMS493, a specific pan-RAR inverse agonist, inhibits M. tuberculosis growth in mice.

Human dendritic cells present Borrelia-derived peptides on HLA-DR molecules.

Borrelia-exposed mo-DCs undergo profound and unique molecular and cellular changes.

Borrelia-exposed mo-DCs may have unique immunoregulatory properties.

There is a role for Rora in Th2 cell development.

Rora CD4-deficient mice expel worms and develop allergic lung inflammation.

Granzyme K expression on innate lymphocytes is associated with a memory-like phenotype.

Granzyme K⁺ cells are enriched in nonlymphoid tissues and express CCR5.

Granzyme K⁺ cells are enriched in tumors and produce IFN-γ but not IL-17a.

Histones produce acute thromboinflammatory responses in vascular endothelium.

Suramin protects small blood vessels from histone-induced damage.

CcGSDMEb-1/2 were cleaved only by CcCaspase-1b.

CcGSDMEb-1/2 exerted toxicity to cells through its N-terminal domains.

CcGSDMEb-1/2 could regulate the secretion of CcIL-1β and the bacterial clearance.

Mass cytometry analysis reveals intratumor immune changes caused by anti-CCR8 therapy.

CCR8⁺ Treg depletion alters intratumor CD8⁺ T cell activation and exhaustion status.

CD8⁺ T cell exhaustion is associated with CCR8⁺ Treg infiltration in human tumors.

GPR56 and granzyme B were significantly coexpressed in circulating T cells.

Increased circulating GPR56⁺ T cells were related to lung cancer progression.

Anti-GPR56 stimulation of GPR56⁺ T cells significantly upregulated granzyme B.

IR-induced immunoproteasomes and APM correlate with tumor T cell infiltration.

Forcing LMP7 expression in an LMP7-negative tumor generates immune rejection.

The irradiation effect on the APM is NF-κB dependent.