Issues

Murine synovial macrophages express pro-Th17 factors during arthritis.

Th17 cells induce CD38⁺ macrophages via TNF-α to further enhance Th17 cells.

TNF-α neutralization or CD38⁺ macrophage depletion reduces IL-17A and arthritis.

Pathogenic Th17 cells show higher ORAI1-dependent SOCE than do nonpathogenic Th17 cells.

NKD2 is important for sustained ORAI1-dependent SOCE in pathogenic Th17 cells.

Type III IFN maintains chronic inflammation during CNS autoimmune disease.

Therapeutic targeting of type III IFN promotes recovery of CNS autoimmunity.

SNPs in REL and BHLHE40 are associated with IL-12 and IL-10 and TB susceptibility.

Genetic associations with secondary traits may identify TB susceptibility factors.

Healthy volunteers were treated with N-803, an IL-15 superagonist.

N-803 was safe and had predictable pharmacokinetics.

N-803 mediated robust pharmacodynamic effects on CD8⁺ T cells and NK cells.

CD47 blockade leads to rapid but resolvable splenic marginal zone B cell depletion.

Anti-CD47 mAb induced CCL2/CCL7 is accompanied by CCR2⁺ monocyte splenic infiltration.

Rap1 binding to talin1 contributes to integrin activation in CD4⁺ T cells.

Both Rap1–talin1 interaction and MRL proteins elicit integrin activation in T cells.

Talin1(R35E,R118E) mutation in T cells protects against experimental colitis.

MAIT cells can show different levels of binding to 5-OP-RU–loaded MR1 tetramers.

Variable tetramer binding levels could be due to coexpression of two TCRα chains.

It is critical to verify MR1 binding of TRAV1-2^– tetramer⁺ cells by gene transfer.

The chitosan nanoparticles could be a useful gene delivery system.

Vaccination of chickens with pcDNA/SBNT-NPs generated a protective immunity.

A single dose of BCG/anti–IL-10R1 generates long-term BCG-specific memory immunity.

A single dose of BCG/anti–IL-10R1 reverses waning protective efficacy of BCG.

Unvaccinated and vaccinated SLAMF1^−/− mice fail to control fungal infection.

SLAMF1 signaling is dispensable for the development of antifungal T cells.

Lack of SLAMF1 signaling results in uncontrolled early infection and inflammation.

Nrf2 deficiency aggravates inflammatory response in ICD.

Nrf2 plays a critical role in ICD through the HO-1/NQO1–ROS–ERK pathway.

PTPRO inhibits granulocyte progenitor proliferation during infection and homeostasis.

mTOR-HIF1α-glycolytic activities are required for granulopoiesis induced by Ptpro^−/−.

pDCs follow a multi-step adhesion cascade to home to VAT that changes upon HFD.

pDCs localize in lymphoid clusters with increased density and activation after HFD.

Blocking the adhesion cascade prevents weight gain and improves glucose tolerance.

TFAM deficiency impairs alveolar macrophage (AM) mitochondria metabolism.

TFAM is required for AM self-renewal and maintenance.

Viral infection leads to decreased AM TFAM expression and mitochondrial fitness.

The age dependency of pediatric asthma is connected to societal viral burden.

Asthmatic phenotypes induced by viral infection attenuate with age in mice.

Alveolar macrophages contribute to the aging out of asthmatic traits in mice.

lncNDEPD1 upregulates PD-1 expression through binding with miR-3619-5p.

Notch1 directly upregulated lncNDEPD1 transcription by physical binding.

Adoptive transfer of lncNDEPD1-knockdown CAR-T cells delayed tumor growth.

A new tool was developed to facilitate the analysis of immune cell migration in vivo.

Computer-assisted annotation improves the accuracy of automatic cell tracking.

We developed a quantitative EIA to detect SARS-CoV-2 IgA/IgG Abs in saliva.

SARS-CoV-2 IgA can be detected in saliva 1 wk after the onset of disease.

Ab fluctuations were different between mild and severe disease cases.