Issues

Constitutively active gp130 in T cells leads to senescence-associated inflammaging.

The JAK/STAT axis is crucial for the development of autoimmunity and thrombocytosis.

The reported mouse line might be used as a model for cellular senescence.

Depletion of mTECs affected the Treg production more strongly than that of DCs.

mTECs, not the cTECs, are the main source of self-Ags transferred from TECs to DCs.

IL-2 produced by recirculating non-Tregs is required for thymic Treg expansion.

CD4 T cell–intrinsic STAT4 expression controls migration to the CNS during EAE.

STAT4 is required for Th17 pathogenicity independent of IL-17A production.

hNSCs induce CD25⁺Foxp3⁺ Tregs from conventional T cells.

This conversion to Tregs is driven by hNSC Ags and not secreted factors.

hNSC Ags require thymic presentation for peripheral Treg conversion.

T_REG population is expanded in severe COVID-19 patients with enhanced apoptosis.

T_REG suppressive function is not altered in patients with severe or mild COVID-19.

T_REG frequency inversely correlates with T cell function in mild COVID-19 patients.

Human CCR6⁺ Th cells lie along an extended, stable continuum of type 17 character.

Type 17 cells show not only environment-inducible but also imprinted plasticity.

Human Th cells with a history of early multilineage activation persist as memory.

Persistent gp130 signaling in T cells causes a bias to T_H17 cell differentiation.

Transgenic mice with continuously active gp130 in T cells develop lung inflammation.

The major S/T phosphorylation on Bcl11b is dispensable for T cell development.

The phosphorylation may regulate Bcl11b protein stability.

Natural microbial exposure expands immune cell progenitors in neonatal mice.

Natural microbial exposure broadly expands mature immune cells in young mice.

Natural microbial exposure enhances early-life host defense.

Mll1 is a positive regulator of T_FH differentiation.

Mll1 regulates expression of LEF-1, TCF-1, and Bcl6.

B. burgdorferi triggers type I IFN responses in macrophages and fibroblasts.

Coiled spirochetes are observed in the cytosol and colocalize with cGAS.

cGAS and STING mediate B. burgdorferi–induced type I IFN responses.

IFN-υ can be activated by IRF1, IRF3, IRF7, and p65.

The ISG repertoire contains major expanded families of AMNTR, GVIN, GBP, RTP, and IFIT.

AMNTR50 negatively regulates the expression of type I, III, and IV IFNs.

Neutrophils, macrophages, endothelial cells, and erythroid precursors produce IL-18BP.

IL-18 indirectly impairs erythropoiesis while favoring myelopoiesis.

High expression of APE1 and APE2 early after activation promote CSR.

After initial activation, APE1 protein dilutes out with cell division.

APE2 remains highly expressed and promotes SHM that is suppressed by APE1.

MHC class I ligands were identified for 12 rhesus macaque KIRs.

Rhesus macaque KIRs interact with three general categories of MHC class I ligands.

Novel KIR interactions were identified with Mamu-AG, -B*045, and -A1*012.

We developed, to our knowledge, a novel technique to specifically identify macrophage subsets in lungs.

We used this method to characterized macrophage phenotypes during lung inflammation.

Development of a novel HPLC method for studying C1q–ligand interactions.

scC1q column binding correlates with biological activity of anti-CD20 IgG isotypes.