Issues

Human pDCs express ATP13A2 in their endolysosomal compartments.

ATP13A2-mediated polyamine transport regulates TLR9/7 activation in pDCs.

ATP13A2 knockdown increases endosomal pH and mtROS, which dampens pDC activation.

UCB monocytes generate mature MoDCs with differences in cytokine and coreceptor profiles.

UCB-MoDCs present avid endocytosis and chemokine-mediated migratory behavior.

The allostimulatory capacity of UCB-MoDCs is reduced for CD4⁺ but not CD8⁺ T lymphocytes.

IL-4 signaling in keratinocytes mediates wound healing.

IL-4 signaling in keratinocytes controls DETC homeostasis.

IL-4 controls keratinocyte production of IL-15.

Treg-specific aPIK3CD expression promotes Teff activation despite increased Treg frequency.

Foxp3-aPIK3CD mice exhibit spontaneous germinal centers and increased Tfh and autoantibodies.

Defective Treg fitness and increased PD-1 contribute to immune dysregulation.

Engineered IgA enhanced neutrophil-mediated cytotoxicity of HPV⁺ HNSCC.

Engineered dimeric IgA outperforms monomeric variants in Fab-mediated mechanisms.

CD147 is critical in target–effector cell cross-talk during neutrophil-mediated ADCC.

M. tuberculosis infected human AMs have a unique transcriptome comparedwith MDMs.

IFNA8, Type I IFN pathway, and DNA sensors are upregulated in TB-infected AMs versus MDMs.

IFNA8 induces a distinct transcriptional program in MDMs compared to other IFNs.

P. yoelii infection induced an elevation in immunosuppressive MDSCs.

GM-CSF/IL-6 activated MDSCs via JAK/STAT3 signaling upon P. yoelii infection.

Depletion of MDSCs enhanced Th1-biased immune responses to P. yoelii infection.

duRNF216 interacts with duTRAF3 and degrades it to downregulate the RIG-I pathway.

duRNF216 targets AIV PB1 and damages viral polymerase assembly and activity.

AIV PB1 targets duRNF216 to attenuate negative regulation of duRIG-I pathway.

Bats generally have shorter IFN-I loci with more unique IFNω-like genes.

IFNω-like genes show the highest basal expression level.

The constitutive IFNω-like genes dominate the antiviral and antiproliferation functionality.

CCR2+ve and CCR1/2+ve monocytes are transcriptionally distinct.

CCR1/2+ve monocytes display a neutrophilic gene signature.

The secretory component D1 CDR3 loop plays an important role in binding to dIgA.

The formation of the SC D1–D3 interface stabilizes SIgA.

JC C-terminal residues influence dIgA assembly and mediate pIgR binding to dIgA.

Bispecifics have a critical end-to-end range for optimal complement activation.

Synthetic biology is useful to evaluate protein engineering to activate complement.