Issues

Prkcd^G510S/G510S mice develop spontaneous lupus-like autoimmunity.

Prkcd^G510S/G510S B cells promote autoimmunity in mice.

PKC-δ acts as a negative regulator of mTOR, and rapamycin can prevent autoimmunity.

CARD19 negatively regulates BCR-CBM complex–mediated TAK1/NF-κB activation.

CARD19 suppresses BCR-induced expression of Egr2/3 and c-Cbl/Cbl-b.

Lack of CARD19 promotes B cell self-tolerance and prevents autoimmunity.

Vaccinated naive and convalescent donors have similar CD4 T cell polyfunctionality.

Convalescents have greater cytotoxic and antiviral spike-specific T cell responses.

KIN1148 is a small molecule compound that binds directly to RIG-I for activation.

KIN1148 serves as an adjuvant for H1N1 and H5N1 influenza virus vaccination.

KIN1148 augments murine and human CD8⁺ T cell responses.

BcfA-adjuvanted vaccines reduce MA10 viral load at 3 mo postbooster.

Respiratory damage is prevented by BcfA-adjuvanted vaccines.

Neutralizing Abs and IL-17⁺CD4⁺ T_RMs are detected at 3 mo postbooster.

IL-4 depletion increased Ag-specific ASCs after antiopioid immunization in mice.

Recombinant oxycodone-specific IgG₁ and IgG_2a display equivalent efficacy.

T cell–derived IL-4 may be a predictive biomarker of antioxycodone vaccine efficacy.

DGKα is required to prevent immune-mediated mortality in LCMV Clone 13 infection.

Immunopathologic host death in DGKα knockout is predominantly CD8 T cell mediated.

Depleting DGKα^−/− CD8 T cells rescues mice from mortality in LCMV Clone 13 infection.

STAT1 protects influenza-primed CD4 T cells from NK cell–mediated deletion.

STAT1 but not STAT4 is needed for Th1 and Th17 functionality in antiviral CD4 T cells.

Engaging STAT1 and STAT4 during priming maximizes protective CD4 T cell capacity.

IFN-γ contributes to control of acute and chronic blood-stage Pcc malaria.

CD4 T cell IFN-γ contributes to control of chronic Pcc blood-stage malaria.

IFN-γ has CD4 T cell independent roles in control of blood-stage Pcc malaria.

Zebrafish mavs is induced by viral infection.

The long isoform of mavs enhances antiviral immune responses.

Mavs-null zebrafish are susceptible to SVCV infection.

A double-β-defensin was identified from an arthropod, L. vannamei.

The expression of LvDBD was regulated by NF-κB.

LvDBD exhibited binding activities to microbes as well as various polysaccharides.

ASFV CD2v binds to STING and inhibits STING translocation to the Golgi apparatus.

CD2v disrupts IFNAR1-TYK2 and IFNAR2-JAK1 interactions to inhibit IFN-I response.

Platelet-derived sTLT-1 plays a crucial role in mediating septic immune dysfunction.

sTLT-1 induces immune activation followed by immune suppression through TLR4/MD2.

Endothelial EGFR controls MCP-1 production and inflammation.

Absence of endothelial EGFR exacerbates insulin resistance in obesity.

Deletion of endothelial EGFR mobilizes circulating monocytes into the liver.

Metabolic zonation exists, but whether innate immunity is zonated remains unclear.

The murine hepatocyte response to endotoxin shows zone-specific characteristics.

Pericentral hepatocyte p50 activation drives CRP induction.

LTA inhibited TLR4-mediated signaling independently of TLR2.

The inhibition of TLR4-mediated signaling was abrogated by the addition of serum or albumin.

LTA promoted formation of inactive TLR4/MD-2 complex dimers.

Bacteria pathogens induce PP2AC and CK2α to modulate hemocyanin phosphorylation.

Dephosphorylated hemocyanin has enhanced antibacterial activity and oxygen carriage.

Thr⁵¹⁷ on hemocyanin is critical for binding with pathogen-associated molecular patterns and antibacterial activity.

A gene in chickens with >80% homology to CR2 from other bird species was obtained.

chCR2 was identified as a distinct immunological marker in chicken B cells.

chCR2 expression varied according to the IBDV infection status.

Decoy peptides derived from the C″ helix of TLR5 or TIRAP TIR inhibit multiple TLRs.

The C″ helix peptides bind to TIR domains of MyD88, TIRAP, and TLR5.

The combination of TheraVac and cGAMP is curative for B16 and M3 melanomas.

The combination therapy induces antimelanoma immune responses.

The combination therapy triggers a Th1 signature with elevated IFN-β in tumor tissue.

In vitro microphysiological systems can recapitulate maternal–fetal immune crosstalk.

The choriodecidual interface regulates feto–maternal immune tolerance.

Maternal infection induces leukocyte infiltration to dislodge immune tolerance.

Mast cell proteases, including tryptase and cathepsin G, can degrade PrP.

An IgE was constructed that could target PrP: anti-PrP IgE.

Anti-PrP IgE was able to effectively activate the human LAD2 mast cell line.