Issues

Cbl-b is induced in IL-15/IL-2/K562–activated primary human NK cells.

Abrogation of Cbl-b enhances cytotoxicity of primary human NK cells.

Multimerization of p67C Ag as nanoparticle increases its immunogenicity.

Vaccine efficacy of p67C Ag increases delivered as nanoparticles.

The combination of cdAMP and Nano-11 has synergistic effects on activation of DCs.

ID immunization with cdAMP/Nano-11 adjuvant induces a robust balanced immune response.

The cdAMP/Nano-11 adjuvant increases uptake of Ag by migratory and resident DCs.

SIRP Abs SIRP-1 and SIRP-2 induce macrophage phagocytosis of cancer cells.

They employ unique mechanisms to disrupt SIRPα/CD47 checkpoint and engage FcγRs.

SIRP-1 and SIRP-2 combine with targeted Abs including anti-CD47 mAb AO-176.

aiPLA2-mediated production of inflammatory lipids drives lung pathological condition during TPE.

IgG cross-linking on eosinophils activates aiPLA2 activity.

Pharmacological inhibition of aiPLA2 improves TPE-associated lung histopathology.

HRG induces the phagocytic activity of human neutrophils against E. coli and S. aureus.

HRG induces shape change of human neutrophils and prolongs the survival time.

The effect of HRG on human neutrophils is mediated by CLEC1A receptor.

Leukocyte influx occurs in specific niches during S. aureus craniotomy infection.

S. aureus craniotomy infection elicits transcriptional diversity in myeloid cells.

PMNs are critical for S. aureus containment but not biofilm clearance.

Intestinal IL-17R signaling plays a beneficial role in infectious colitis.

Intestinal IL-17R signaling regulates ASC generation and transport of SIgA.

Expression of oxidases during infectious colitis requires intestinal IL-17R.

Replication-competent VACV inhibits skin DC migration to draining lymph node.

The VACV-suppressive effect is a general phenomenon of VACV infection in the skin.

VACV can access the lymph node in the absence of DC transport and prime CD4⁺ T cells.

TNF downregulates IFN-α and TNF production by human pDCs.

TNF downregulates IRF7 and NF-κB pathways and upregulates Ag processing in pDCs.

TNF enhances Ag presentation and T cell activation properties in pDCs.

eCIRP induces NET formation, causing inhibition of efferocytosis during sepsis.

NE of NETs disrupts α_vβ₃ and α_vβ₅ integrins in macrophages to inhibit efferocytosis.

Hyperglycemia promotes trained immunity of monocytes/macrophages.

MLL mediates hyperglycemia-induced trained immunity.

Loss of ADAP enhances TLR4-mediated M1 polarization via attenuating STAT3 activation.

LPS triggers ADAP Y571 phosphorylation, which is required to prime STAT3 activation.

ADAP modulates STAT3 phosphorylation selectively via IL-6 signaling.

Nonadherent monocytes produce more TNF and IL-1β upon LPS stimulation.

Adherent, but not nonadherent, monocytes induce glycolysis upon stimulation.

Treatment with 2DG, but not glucose deprivation, influences monocyte functions.

Ablation of the IL-23/T17 axis restrains the skin inflammation in Card14^E138A/+ mice.

CBM complex in keratinocyte initiates psoriasis-like skin inflammation.

MALT1 paracaspase activity could be a promising therapeutic target for psoriasis.

NK cells are differentially inhibited by HLA-A^Bw4 interactions with KIR3DL1.

Residues within the HLA class I α2 helix contribute to defining KIR3DL1 ligands.

KIR3DL1 binds HLA-A^Bw4 ligands via the same contacts as HLA-B^Bw4 ligands.

We have identified a family of modified DNA aptamers that bind to human factor B.

Studies on these modified aptamers reveal how they inhibit C3 convertase formation.

These modified aptamers may prove useful for therapeutic inhibition of factor B.

Most maternal (28-wk gestation) 25(OH)D₃ levels were above 50 nmol/l.

Maternal 25(OH)D₃ levels were positively associated with cord blood Treg levels.

Cord blood 25(OH)D₃ levels were associated with activated Treg levels.

A computational model of the signaling network for macrophage activation is developed.

Conflicting cues induced a “mixed” activation state not seen with single cues.

Knockdown simulations predict mechanisms underlying mutual inhibition or activation.

MyD88 costimulation in donor CD8⁺ T cells improves the graft-versus-tumor effect.

MyD88-costimulated CD8⁺ T cells are more activated with improved cytotoxic function.

Moderate exercise reduces inflammaging, liver tumors, and chronic liver disease.

Key molecular changes include lipid metabolism, oxidative damage, and senescence.

Increased NAD⁺, sirtuin activity, and inflammatory and metabolic reprogramming occur.