Issues

Canonical autophagy drives TAP-independent Ag cross-presentation.

LC3A/B-positive vesicles associate with the phagosome.

Proteasomes localize within the lumen of LC3A vesicles associated with phagosomes.

Hypoxia impairs the activity of the epigenetic regulator UTX in CD4⁺ T cells.

UTX impairment protects against colonic inflammation in an IBD mouse model.

UTX loss downregulates inflammatory Th1 and increases suppressive Treg responses.

Normal and malignant B cells lacking CD53 have impaired CXCL12-directed migration.

CD53 is a novel binding partner of CXCR4 in B cells.

CD53 promotes CXCL12/CXCR4 signaling and marrow homing in B cells.

Fosl2 loss skews HSCs towards myeloid cell differentiation.

Fosl2 loss induces osteopetrosis in mice, causing bone marrow failure.

The initial pathology of T1D is located outside the islet basement membrane.

A postcapillary venule–associated cell population expresses MHC class II molecules.

An extraislet tertiary lymphoid structure is necessary for progression of disease.

COVID-19 presents low percentages of perforin-expressing NK cells.

This was not linked to disease severity but anticorrelated with NK degranulation.

A primary perforin deficiency does not seem to be a driver of COVID-19.

CTLA-4 suppresses T cell activation, proliferation, and effector function of tilapia.

Tilapia CTLA-4 competes with CD28 for B7 binding.

CTLA-4 inhibits mTORC1/c-Myc axis–controlled T cell glycolysis and immunity.

Eos positively regulates cytotoxic programming in CD4⁺ T cells.

Eos promotes IL-2 and IL-15 cytokine receptor expression.

Aiolos antagonizes STAT5-dependent induction of Eos expression.

Disabling CD55 globally accelerates the growth of multiple cell types.

Potentiated C3ar1/C5ar1 signaling integrates with the signaling of receptor RTKs.

DNA-reactive B cells require CD40 signaling to mount an autoantibody response.

Bystander CD4 T cells can provide T cell help to support an autoantibody response.

Enhanced PI3K signaling makes autoreactive B cells receptive to bystander T cell help.

T. gondii infection induces IL-1β release from human peripheral blood monocytes.

Caspase-8 is not required for IL-1β cleavage but is critical for IL-1β release.

IL-1β is released via a pathway that is independent of cell death, GSDME, or ATG7.

This study highlights a unique C1s/MASP-2 interaction with the vWF domain of C2.

This insight reveals a previously unexplored aspect of complement activation

CLEC-1 represses CXCL-2–dependent neutrophil recruitment.

CLEC-1 prevents additional tissue damage following injury.

Astaxanthin reduces HSV-1–induced lipid peroxidation and STING carbonylation.

Astaxanthin promotes STING translocation to the Golgi apparatus and oligomerization.

Astaxanthin selectively enhances the cyclic GMP-AMP synthase–STING pathway and inhibits HSV-1 replication.

FcγRIII participates in cytokine production and bacterial killing in flounder B cells.

FcγRIII can rebind onto the surface of flounder B cells.

Platelet-derived ADAM17 can regulate the shedding of FcγRIII from flounder B cells.

We solve the crystal structure of a fish type I subgroup d IFN, LcIFNd.

LcIFNd activates the conserved JAK-STAT pathway by binding with CRFB1 and CRFB5.

We identify key amino acids of LcIFNd that interact with receptors.

The mice overexpressing CD109 were resistant to bleomycin-induced pulmonary fibrosis.

CD109 protein inhibits pulmonary fibrosis development via inhibiting TGF-β signaling.

CD109 might be a novel therapeutic candidate for treating pulmonary fibrosis.

Single-cell sequencing revealed that IDO1 inhibition activates JAK2-STAT3 in tumor cells.

Coinhibition of the IL-6/JAK2/STAT3 pathway and IDO1 effectively reduced tumor growth.

Alamar NULISAseq demonstrated the highest overall detectability.

Alamar and Olink showed the greatest concordance in pairwise platform comparisons.

Our study reinforces previous findings related to severity in COVID-19.