Issues

CD36 selectively binds to avirulent T. gondii and mediates macrophage tropism.

CD36 is not required for Th1 immune resistance but is vital for tissue tolerance.

The ROP-18 virulence factor negatively regulates CD36 binding to Toxoplasma gondii.

CCR6 is upregulated on CNS-resident B cells but is not required for CNS entry.

B cell expression of CCR6 increases nonspecific plasma cell output following MOG immunization.

B cell expression of CCR6 is not required for induction of B cell–dependent EAE.

AD has been associated with NK cell dysfunction.

Individuals with KIR2DS1, KIR2DL5, and KIR2DS5 are more likely to have AD.

These KIR genes and KIR-associated HLA epitopes increased the risk of AD.

LNSC MHC-II drives conversion of CD8 T cells to CD4 CI-T_reg cells.

LNSC coculture helps generate and expand CI-T_reg cells in vitro.

CI-T_reg cells expanded in stromal cell coculture suppress colitis in mice.

Fc galactosylation enhances complement activity of WT IgG1, but not hexameric IgG.

Fc galactosylation improves hexamerization potential of IgG1.

P2Y₆ deficiency enhances the maturation and functions of NK cells.

P2Y₆ deficiency promotes the expression of T-bet in NK cells.

P2Y₆ deficiency increases the antitumor activities of NK cells.

Exposure of P5 at the surface of NTHi positively correlates with C4BP binding.

C4BP bound to the bacterial surface retains its complement inhibitory capacity.

C4BP binding to P5 is important for NTHi serum resistance.

Malaria-specific T cells can enter the brain parenchyma near the onset of ECM.

Infiltration of T cells into the brain parenchyma contributes to cerebral pathology.

Memory T cells can form within the brain parenchyma after malaria infection.

T cells from COVID-19 patients display less complex N-glycans at diagnosis.

IL-2 is a putative driver of glycan switch in COVID-19 patients.

DC-SIGN expression in monocytes at diagnosis predicts poor disease course.

Mice expressing a mutated form of GFI1 show signs of inflammation.

Mutated GFI1 can still occupy genes, leading to a specific histone mark landscape.

The PP4 complex modulates the IMD-NF-κB–dependent immune response in Drosophila.

Loss of PP4 leads to exacerbated IMD-NF-κB signaling and a reduced lifespan.

Genetic and coimmunoprecipitation data propose an interaction between PP4 and the IKK complex.

Crystalline silica induces an immunometabolic response in RAW 264.7 macrophages.

Silica induces macrophages activation without requiring LPS priming.

Mitochondrial complex II is crucial for macrophage response and survival to silica.

Anticoagulation by GPRP allows thrombin generation in human whole blood.

Thrombin does not cleave plasma C5 in its native form.

pH-induced C5 conformational change allows thrombin-mediated cleavage of C5.

A 15 aa IKIP peptide (46–60 aa of IKIP) inhibits IKK activation.

IKIP peptide inhibits IKK activation via disruption of NEMO binding to IKKα/β.

Administration of IKIP peptide attenuates inflammatory responses in vivo.

PEP-619WW mice have superior control of immunogenic tumors.

PEP-619WW mice had increased tumor-infiltrating lymphocytes.

Tumor-infiltrating lymphocytes have a more activated phenotype in PEP-619WW mice.

ILC1s are enriched in the bone marrow of patients with AML and leukemic mice.

AML promotes ILC1s in part via AHR-mediated skewing of ILC precursor development.

GM-CSF, TGF-β, and rosiglitazone induced the generation of AM-like cells.

AM-like cells serve as a tool for studies of AM differentiation and function.