Issues

MASP-1 is required for physiological LP activation.

MASP-3 circulates predominantly in an active form regardless of the role of MASP-1.

MASP-3 is pivotal for physiological AP activation via activation of FD.

α4 integrins are dispensable for cDCs and pDCs to populate the CNS in steady-state.

Itga4^−/− moDCs have a competitive disadvantage to accumulate in the inflamed CNS.

Accumulation of CD11b⁺CD103⁺ DCs in gut lamina propria is dependent on α4 integrins.

Vitamin D concentrations in COPD patients were lower than concentrations in controls.

TGF-β/Smad signaling and EMT were increased in COPD patients compared with controls.

Vitamin D status was inversely correlated with EMT in COPD patients.

Intracellular cAMP regulates CD39-dependent adenosine production in Tregs.

Extracellular cAMP directly participates in Treg-derived adenosine production.

Increasing the intracellular cAMP level improves the therapeutic efficacy of iTregs.

TRAF5 deficiency accelerates wound healing by promoting activation of pDCs.

TRAF5 controls proinflammatory cytokine production by pDCs via IRF5.

IL-33 is expressed during early B cell development in both mice and humans.

Deficiency of IL-33 promotes B cell fitness via a cell-endogenous mechanism.

IL-33 expression is modulated in B cell malignancies.

Fetal and adult blood Vγ9Vδ2 T cells express a different CDR3 repertoire.

The postnatal thymus produces a small number of Vγ9Vδ2 thymocytes.

Adult blood Vγ9Vδ2 T cells are derived from postnatal Vγ9Vδ2 thymocytes.

Trout have limited IgM and IgT repertoire diversity in NALT.

Intranasal vaccination in trout triggers systemic and mucosal Ig response.

IgM and IgT respond to i.p. and intranasal bacterin vaccination.

HR supports germinal center B cell survival and Ab affinity maturation.

HR is active at the hypermutating Ig locus and influences the SHM mutation pattern.

The magnitude of A:T mutagenesis during SHM of the Ig V region increases over time.

Human CD4 T cells have limited cross-reactive memory to avian H7 proteins.

CD4 T cell help can be provided to B cells with novel H7/H3 chimeric vaccines.

IL-6R signaling on T cells is essential for controlling chronic viral infection.

IL-6R signaling on T cells is required for optimal Ab development.

IL-6 signaling on T cells regulates ICOS expression on Tfh cells.

Inflammatory agent exposure causes c-Abl to interact with and phosphorylate PARP1.

Tyrosine phosphorylation of PARP1 is crucial for NF-κB activation and gene expression.

BACH1 and myeloid HMOX1 are required for complete muscle regeneration upon acute injury.

BACH1–HMOX1 axis is required for coordinated in situ MF phenotype switch.

BACH1 regulates inflammatory and repair gene modules in MFs during tissue injury.

The transcription of IL-7–AS is dependent on the NF-κB/MAPK pathway.

IL-7–AS promotes the expression of CCL2, CCL5, CCL7, and IL6.

IL-7–AS interacts with p300 and SWI/SNF complex.

YIPF5 positively regulates STING-mediated IFN production signaling.

YIPF5 is essential for antiviral response against DNA viruses.

YIPF5 facilitates STING trafficking by recruiting STING to COPII-coated vesicles.

Heme induces complement-dependent thromboinflammation in human whole blood.

Heme-induced proinflammatory cytokines and tissue factor are C5 dependent.

Combined inhibition of C5 and CD14 attenuate prothrombin cleavage.

A negative feedback loop, integrin–PI3K–ARAP3–integrin, controls integrin inactivation.

Integrin inactivation promotes neutrophil transendothelial migration and recruitment.

Retinoids enhance cathelicidin antimicrobial peptide expression during adipogenesis.

The action of retinoids is dependent on hypoxia-inducible factor 1-α.

The capacity to induce cathelicidin may explain some therapeutic effects of retinoids.

NAD⁺ depletion attenuates TLR4 signal transduction in primary human monocytes.

The mechanism involves inhibition of protein phosphorylation in the signal cascade.

The proteins in the signal pathway are not quantitatively changed by NAD⁺ depletion.

Influenza vaccination primes myeloid cells for enhanced cytokine secretion.

Vaccine-enhanced myeloid cytokines boost NK cell responses to influenza virus.

Peptides with β-amino acids can bind tightly to MHC-II and activate TCR signaling.

Incorporation of β-amino acids enhances resistance to degradation by protease(s).

A selected β-amino acid–containing peptide stimulated T cells in mice.

KIR3DL1 allotypes impact the development of Behçet disease.

This association appears to be independent of the effect of HLA-B*51.

Different KIR3DL1 allotypes are associated with mucocutaneous and ophthalmic disease.

TRIM58 interacts with TLR2, negatively regulating its expression in myeloid cells.

Myeloid cell Trim58 deficiency increases susceptibility to acute colitis via Tlr2.

Mucosal expression of human TRIM58 is reduced in active ulcerative colitis.

DN B cells are abnormally elevated in MS patients but have the same origin as in HC.

DN B cells resemble CSM B cells but appear to be at an earlier maturation state.

DN and CSM B cells undergo unique differentiation pathways.

EBV latency III B cells display an immunosuppressive profile similar to Bregs.

They repress proliferation of T cells and promote expansion of cTregs and uTregs.

Expansion of Tregs depends on PD-L1 whose expression depends on the EBV oncogene LMP1.