Issues

SARS-CoV-2–induced mortality in K18-hACE2 mice is dependent on transgene dose.

Low hACE2 copy number mice exhibit reduced viral replication in the lung and brain.

One-copy hACE2 transgenic mice are an improved model of SARS-CoV-2 infection.

Anti-rituximab Abs may cross-react to ocrelizumab, not to obinutuzumab or ofatumumab.

Obinutuzumab or ofatumumab is a safe alternative in case of Abs to rituximab.

Augmenting Vβ rearrangement facilitates analysis of biallelic Tcrb gene assembly.

Cyclin D3 mediates TCRβ protein–signaled feedback inhibition of Vβ recombination.

Alternatively spliced variants of CD3ζ affect T cell development and activation.

CD3ι-expressing T cells develop and activate normally, similar to cells expressing CD3ζ.

Mice reconstituted with CD3θ or CD3η have severe thymic defects.

Ab-7 obtained by phage display library plays a favorable antiviral role.

Antigenic epitope ESQEFTTLTSH is pivotal in Ag–Ab binding.

Peptide vaccine KLH-G2^10–20 induces a strong and specific immune response.

Asymptomatic MHV-1 dose provides protection to high-dose MHV-1 rechallenge.

Neutralizing Abs provide protection to high-dose viral challenge.

Sepsis, as a comorbidity, increases susceptibility to MHV-1 infection.

Preclinical trial testing efficacy of RAGE-Ig for COVID-19 in mouse and hamster is reported.

Antiviral and anti-inflammatory therapeutic effects of RAGE-Ig were found for COVID-19.

IL-2 sustains Th1 responses in the later stages of the antiviral response.

Differential exposure to IL-2 shapes the memory T cell compartment.

IL-2 is required to sustain Th1 responses even in the absence of TCF-1.

Incomplete caspase-1 processing in hepatocytes is due to lower expression of ASC.

Enhancing ASC expression resulted in complete caspase-1 processing in hepatocytes.

This led to increased pyroptotic death in hepatocytes and better control of malaria.

Schistosome infection impairs bone marrow HSC function after serial transplantation.

Infection blocks marrow erythropoiesis and increases spleen erythropoiesis.

Hematopoietic activity is increased in the livers of infected mice.

Immunization with the GFP-DDDHA strain protects against secondary infection.

NK cells expand and develop a memory subset during immunization.

Memory NK cells rapidly proliferate and are highly cytotoxic in the recall response.

CD4 T cells express CX3CR1 at the site of inflammation during helminth infection.

CD4 T cells that maintain CX3CR1 expression persist in the peripheral tissue.

CD4 T cells that express CX3CR1 are a transcriptionally heterogeneous population.

OnCL-K1 significantly reduced the proliferation of pathogens.

OnCL-K1 associated with OnMASPs to initiate the lectin complement pathway.

OnCL-K1 promoted phagocytosis and killing of macrophages with OnCD93 interaction.

CD13 is a negative regulator of macrophage fusion and giant cell formation.

Implant-induced FBGC formation and implant site fibrosis are increased in CD13^KO mice.

CD13 controls fusogen expression and actin protrusion to regulate fusion.

LPS stimulation induces CHTOP expression in microglia.

CHTOP regulates the expression of cell metabolism and inflammation-related genes.

Knockdown of CHTOP in microglia increased neuronal viability.

A1 was identified as a candidate C1s binder through an artificial intelligence–based virtual screen.

A1 inhibits C1s dose-dependently with low micromolar potency in functional assays.

Structure of C1s inhibited by A1 suggests strategies for next-generation A1 analogs.

The CMA-associated microbiota is enriched for LPS⁺ bacteria.

The CMA microbiota is associated with intestinal inflammation.

Proinflammatory responses in CMA-colonized mice depend on TLR4 in CD11c⁺ APCs.

IFN-β upregulates HLA-E and PD-L1 expression through the JAK/STAT/IRF7 pathway.

IFN-β–induced HLA-E protects HK-2 cells from allogeneic NK cell attack.

BDMC enhances IFN-β–induced HLA-E and PD-L1 expression in vitro and in vivo.

The abnormal expression of METTL14 is related to glycolysis of tumor cells.

PD-1 expression in M2 macrophages is negatively correlated with phagocytosis.

Tumorous glycolysis might be the potential mechanism for the function of macrophages.

HDACis directly promote expression of activation-associated genes in T cells.

In the TME, HDACis promote both T cell activation and exhaustion.

HDACis mediate expansion of immunosuppressive myeloid populations.