Issues

Pulmonary fibrosis entails a transcriptional downregulation of Map3k8 expression.

Map3k8 suppress pulmonary fibrosis via Cox-2–mediated PGE₂ production.

NHERF1 promotes mast cell activation following FcεRI stimulation in vitro.

NHERF1 regulates IgE-mediated, mast cell–dependent anaphylactic reactions in vivo.

NHERF1 localized to the mast cell nucleus following IgE/Ag stimulation.

GSK3–c-Myc–IRF4 regulatory axis induces CD138⁺ Ab-secreting cell formation.

GSK3 inactivation facilitated the LZ to DZ transition via increasing Foxo1.

Spatiotemporal control of GSK3 activity may be a key regulator of the GC reaction.

The onset and evolution of EAE in C57BL/6 mice is significantly delayed by ILT3.Fc.

ILT3.Fc inhibits T cell production of IL-17 and IFN-γ and migration through BMEC.

Deletion of CD8 T cells abrogates the inhibitory effect of ILT3.Fc.

Pulmonary mucosal CD8 T cells are highly differentiated, activated, and exhausted.

BAL versus blood CD8 T cells showed lower perforin/granzyme B expression.

BAL CD8 T cells display reduced target killing ability compared to blood CD8 T cells.

Salmonella infection leads to NAIP/NLRC4 and NLRP3 inflammasome activation.

Flagellin activates the NAIP/NLRC4 and NLRP3 inflammasome in human macrophages.

Flagellin mediates NLRP3 activation in a ROS- and/or cathepsin-dependent manner.

Mo/MΦ proliferate at higher rates in wounds of diabetic compared with nondiabetic mice.

CCL2/CCR2 signaling promotes wound Mo/MΦ proliferation in mice.

Spike-reactive T cells are present in all convalescent COVID-19 patients.

NCAP and VEMP are possible targets for treatment and diagnosis.

SARS-CoV-2–reactive T cells cannot be detected in unexposed individuals.

Homeostatic turnover generates heterogeneity in cell age among naive group 1 ILCs.

Turnover of tissue-resident ILC1s is slower than that of circulating NK cells.

Older NK cells mount more robust adaptive responses during CMV infection.

In fibrosing mediastinitis, CD4⁺CD4⁺CTLs accumulate in lesions.

CD4⁺CTLs in the blood of patients respond to H. capsulatum Ags in vitro.

Vitamin D was decreased and inflammation was increased in COPD patients.

NF-κB and AP-1 signaling pathways were activated in COPD patients.

Vitamin D was inversely correlated with inflammatory signaling in COPD patients.

S100a8- and S100a9-deficient mice have worsened psoriasis.

S100A8 and S100A9 inhibit IL-17 production.

MHC-II ubiquitination–mutant spleen DCs are functionally defective.

MHC-II ubiquitination–mutant DCs have an altered gene expression profile.

DC activation reverses the functional defects in MHC-II ubiquitination–mutant DCs.

mirn23a miRNAs repress inflammatory signaling in myeloid progenitors.

mirn23a^−/− macrophages have enhanced M2 polarization and decreased responses to LPS.

mirn23a^−/− macrophages enhance the growth of syngeneic tumors in vivo.

Simultaneous aerosol and i.m. immunization reduces viral load and pathology.

Simultaneous immunization induces strong protective local and systemic responses.

The hierarchy of NP-specific T cells in blood does not reflect local lung responses.

Tocilizumab could prolong survival among hospitalized patients with severe COVID-19.

Tocilizumab weakens the inflammatory response while sustaining immune responses.

During the tocilizumab treatment, no severe adverse drug reactions were reported.

Vitamin D₃ reduces FcεRI expression on epidermal DC in atopic dermatitis.

This is independent of activation and results in impaired FcεRI-mediated function.

Vitamin D₃ causes dissociation of PU.1 and YY1 from the FcεRI α-chain promotor.

PPRV P protein inhibits type I IFN production.

PPRV P protein interacts with IRF3 to block the interaction between TBK1 and IRF3.

The 1–102 region of P protein is critical for the antagonistic function of P protein.

Sema3E suppresses CD11C⁺ cells and T cell functions during L. major infection.

The deficiency of Sema3E leads to enhanced resistance to L. major infection.