Issues

Cytokines driving ABC emergence have stage-specific functions.

ABCs differentiate de novo in the liver.

The rate of the MCAM⁺CD161⁻Th17 subset was positively correlated with psoriasis severity.

The MCAM⁺CD161⁻Th17 subset expressed CD83 more frequently than did the other subsets.

CD83 led to Tc17 proliferation, and exogenous IL-17A drove IL-17A production of Tc17.

Reference functions describe human T lymphocyte densities as a function of age.

Lymphocyte counts linearly increase for the first half a year before declining.

CD4 and CD8 T cell percentages follow a “wavy” trajectory over time.

A single Tox mRNA encodes two proteoforms with different N-termini.

Truncated TOX is translated by leaky scanning and regulated by cell context.

Alternative TOX proteins have overlapping but distinct effects on gene expression.

ZIKV infection inhibits Twist1 expression and trophoblast migration.

Twist1 interacts with IRF9 and provides protection against ZIKV infection.

IFN-β inhibits Twist1 expression.

CXCR4 mutation in WHIM patients and mice elevates blood CD4/CD8 T cell ratios.

WHIM CD8 T cells accumulate in the thymus and bone marrow of mice.

T cell lymphopenia in WHIM mice is ameliorated by the CXCR4 antagonist AMD3100.

S- and N-predicted epitopes are antigenic for sera of infected patients.

Vaccination with rBCG leads to neutralization against virus and cytokine responses.

rBCG immunization protects K18-hACE2 mice against SARS-CoV-2 challenge.

Prenol, but not vitamin C, prevents the binding between spike S1 and ACE2.

Prenol, but not vitamin C, reduces the entry of pseudo–SARS-CoV2 into the cells.

Oral prenol protects mice from SARS-CoV-2 spike S1 toxicity.

Memory generation from CD4 effectors is proportional to their avidity for Ag/APC.

TCR avidity regulates autocrine IL-2 and thus regulates their survival and function.

Influenza infection activates APCs to express CD25 and transpresent IL-2.

Diabetes exacerbates MI/R injury.

The major trigger of increased P2X7 was the recruitment of monocytes and macrophages.

Administration of antagonist before or after MI/R alleviates myocardial injury.

Gasdermins play an essential role for biogenesis of apoptotic cell–derived exosomes.

GSDME-mediated calcium influx results in recruitment of the ESCRT-III complex in MVBs.

The ESCRT-III complex contributes to formation of ILVs in MVBs of dying cells.

Plasma RNAs are upregulated and miRNA profiles altered in severe blunt polytrauma.

Plasma RNAs and ex-miRNAs of injured mice activate innate immunity via TLR7.

TLR7 KO mice have lower blood cytokines and reduced liver and lung injury in trauma.

Cyclic stretch increased the secretion of exosomes from HPDLCs.

The exosomes enhanced the force-related periodontal inflammation.

The exosomes induced M1 polarization of macrophages via miR-9-5p/SIRT1/NF-κB.

LPS triggers upregulation of CCL3, CCL4, CXCL2/3, and CXCL10 genes.

In ALI, myeloid cells with CCR1, CCR3, CCR5, and CXCR2 receptors are recruited.

LPS regulates miRNAs that target the induction of chemokine genes.

Radical nephrectomy results in increased cytotoxic function of peripheral lymphocytes.

H1A treatment of PBMCs promotes cytotoxic killing of tumor cells.

H1A induces expansion of effector CD8 T and NK cells.

This method expands the number of fluorophores that can be used in histology.

Histoflow cytometry can accommodate high-parameter single-cell analysis.

Histoflow cytometry can identify meaningful biological differences.