Issues

Severe COVID-19 is associated with reduced A-to-I editing of Alu dsRNAs.

Infection of dendritic cells with COVID-19 causes reduced A-to-I editing.

Unedited, but not edited, Alu dsRNAs activate IRF and NF-κB responses.

SP subunits are not upregulated in IP-deficient mice during viral infection.

IP is not required to control protein homeostasis during viral infection.

There is no evidence for proteotoxic stress in IP-deficient mice during viral infection.

BVDV-1– and -2–immunized cattle developed cross-reactive CD8⁺ T cells.

IFN-γ–inducing CD8⁺ T cell epitopes were identified from various BVDV Ags.

CD8⁺ T cell epitopes are highly conserved across >200 BVDV-1 and -2 strains.

PPP2R2A promotes Th1 and Th17 but not Treg cell differentiation.

PPP2R2A deficiency impairs GEF-H1/RhoA/ROCK pathway in Th1 and Th17 cells.

PPP2R2A deficiency in T cells mitigates experimental autoimmune encephalomyelitis.

Antiribosomal P protein Abs induced depressive behavior and anxiety in mice.

Brain and serum tryptophan were decreased in mice with behavioral deficits.

Serum tryptophan was decreased in SLE patients with anti-P Abs or with NPSLE.

A TNFR2 agonist, R2agoTNF, selectively and preferentially expands Tregs in mice.

Structural optimization of R2agoTNF increased Tregs via enhanced TNFR2 signaling.

scR2agoTNF-Fc is a potential drug to suppress contact hypersensitivity.

EPO exerts a significant therapeutic effect on the DAH murine model.

EPO protects against DAH by regulating macrophage polarization via the EPOR/JAK2/STAT3 axis.

BALM affects trout B cell functionality in a manner similar to BAFF and APRIL.

Evidence suggests that BALM signals through the same receptors as BAFF and APRIL.

PDK1 is required for Treg cell suppressive function.

PDK1-deficient Treg cells have impaired NF-κB signaling.

Forced activation of NF-κB rescues the phenotype of Foxp3^YFP-cre Pdk1^f/f mice.

FXIa cleaves CFH at the R341/R342 bonds at the end of the CCP 6 domain of CFH.

FXIa reduces CFH cofactor and decay‐accelerating activity and binding to ECs.

CFH binds FXI and inhibits FXI activation by either thrombin or FXIIa.

CD154-EM mutant is resistant to the spontaneous and induced cleavage from T cells.

Spontaneous and induced cleavage of CD154 from T cells is mediated by ADAM10/ADAM17.

The cleavage-resistant CD154 is a more prominent stimulant than cleavable CD154-WT.

Glycolipid-adjuvanted vaccine activates iNKT cells to support humoral immunity.

Nanoparticle delivery of glycolipids avoids iNKT anergy and allows adjuvant dose sparing.

iNKT cells can either support or suppress vaccine responses, depending on context.

Construction of a PfMSP2/8 immunogen improved vaccine potential.

GLA-SE as adjuvant increased titer and functionality of vaccine-induced IgG.

Individual components of a trivalent malaria vaccine retained immunogenicity.

OTUD1 deubiquitinates CARD9.

OTUD1 positively regulates CLR-induced signaling and cytokine production.

OTUD1 protects mice against C. albicans–induced fungal infection.

ASFV MGF-505-7R inhibits cGAS–STING signaling.

MGF-505-7R–deficient ASFV was fully attenuated in pigs at a dose of 10 HAD₅₀.

PVB inhibits GM-CSF–induced neutrophil priming.

PVB may be used “off-label” to improve the survival of patients with sepsis.

HSV-1 infection induces a strong IFN-λ response at the corneal epithelial surface.

IFN-λ differentially regulates antiviral and inflammatory responses in the cornea.

rIFN-λ treatment suppresses HSV-1–induced corneal immunopathology.

Heme induces oligomerization of caspase-1, caspase-4, and caspase-5.

Heme-induced IL-1β release requires both caspase-4 and caspase-5.

Caspase-4 is the primary effector of heme-induced cell death.

IFN-I signaling in CLPP-deficient cells and tissues depends on cGAS and STING.

CLPP-deficient cells are resistant to DNA and RNA viruses because of elevated ISGs.

CLPP-deficient cells exhibit mitochondrial DNA stress and release into the cytosol.

M. smegmatis were killed by human neutrophils more slowly than other bacteria.

Phagosomal M. smegmatis kept their mycothiol reduced despite HOCl exposure.

Sensitizing mycobacteria to killing by HOCl would aid destruction by neutrophils.

Zebrafish caspy2–GSDMEb axis contributes to neutrophil pyroptosis in vivo.

Depletion of caspy2 or GSDMEb impairs the process of NETosis.

Pyroptosis-gated NETosis plays a critical role in teleost innate immunity.

Neutrophils actively internalize pulmonary surfactant during cigarette smoke exposure.

Absence of neutrophils alters surfactant homeostasis during smoking.

Absence of neutrophils exacerbates the proinflammatory response to smoking.

Cell stress induces the expression of EGOT via the PI3K/AKT, MAPK, and NF-κB pathways.

EGOT favors the expression of PI3K/AKT target genes required for cell proliferation.

EGOT supports TBLR1 expression, contributing to transcription of NF-κB target genes.

LL neutrophils express genes of peptidase inhibitor families.

The PI3 gene encoding elafin is the most highly expressed gene by LL neutrophils.

Elafin is produced because of a synergism between GM-CSF and TNF via C/EBPβ and NF-κB.

Human HLA-reactive mAbs OK4F9 and OK4F10 cross-react to Mamu-B*008:01.

Human mAb MUS4H4 shows a more complex cross-reactivity in relation to Mamu allotypes.

Presence of IL-1α in melanoma makes the disease resistant to immunotherapy.

IL-1 pathway blockade enhances the efficacy of CD40 agonist therapy.

IL-1 pathway blockade improves response to therapy through elimination of PMN-MDSCs.