Issues

αβ T cells are required for Ab production and clearance of Bartonella infection.

CD1d- and MR1-restricted T cells can compensate for a lack of MHC-II.

Unconventional T cells can act as helper cells in systemic bacterial infections.

IL-27 gene therapy dramatically inhibits lethal autoimmunity in Scurfy mice.

The therapeutic effect largely depends on IL-27–induced expression of IL-10.

Endometriotic lesions secrete exosomes expressing MICA/B, ULBP1–3, FasL, and TRAIL.

These exosomes downregulate the NKG2D cytotoxic pathway and upregulate apoptosis.

This promotes immune escape by suppressing cytotoxicity and killing lymphocytes.

TLR10 is constitutively expressed on human pDCs, B cells, and monocytes.

TLR10 engagement inhibits cytokine production and IRF7 translocation in pDCs.

TLR10 activation induces SOCS3 expression via STAT3 phosphorylation in pDCs.

CD39 is expressed on human and murine CD8⁺ T_RM cells.

Virus-specific CD39⁺ T_RM cells are functional ex vivo.

Inhibiting CD39 during in vitro T cell priming enhances T_RM cell establishment in mice.

Activation of AHR in lung epithelia with FICZ suppresses proinflammatory responses.

Lung AHR suppresses TGFβ-mediated EMT transitions and enhances epithelial barrier function.

AHR plays a protective role in epithelial lung injury and repair processes.

Allotype-specific ELISA allows one to distinguish maternally derived and neonate-derived Ab responses postvaccination.

Breastfeeding from an immune dam limits vaccine immunity in the neonate.

Sepsis affects IFN-γ production by CD8⁺ T cells in a cell-intrinsic manner.

Chromatin remodeling at the Ifng locus is impaired in CD8 T cells exposed to sepsis.

Nemo SQ motifs are not required for overall normal B/T-cell development in mice.

Nemo SQ motifs are dispensable for DSB-dependent gene expression changes.

HEB enables β-catenin block in DP thymocytes; its removal restores thymic selection.

β-Catenin directs HEB to new sites, altering thymic selection and cell cycle genes.

Block reversal is TCF-1 independent, indicating unique HEB functions.

Structural variation in IGH limits effectiveness of a single linear genome reference.

Structural variation in IGH limits accuracy of short-read epigenetic data.

Long-read technologies provide haplotype-resolved genomic information in IGH.

Mutations in the Fc portion of anti-fentanyl mAbs increase binding to hFcRn in vitro.

Fc mutant mAbs reduced fentanyl distribution to the brain.

DF215 mutant showed highest affinity for hFcRn and most prolonged half-life in vivo.

Intranasal BCG vaccination increases lung-resident CD3⁻NK1.1⁺CD69⁺CD103⁺ cells in mouse lungs.

Adoptive transfer of lung-resident CD3⁻NK1.1⁺CD69⁺CD103⁺ cells significantly reduced Mtb burden.

Lung-resident CD3⁻NK1.1⁺CD69⁺CD103⁺ cells expand and provide protection against Mtb Infection.

Patient Ab from 2020 Wuhan infection maintains Fc function across evolving strains.

This protective, non-neutralizing anti–N-terminal domain mAb functions against BA.2.86-JN.1.

JN.1 exhibits attenuated virulence with weak in vivo infection in K18-hACE2 mice.

MtbΔpknF induces higher IL-1β production and pyroptosis in BMDCs.

Inflammasome activation is dependent on NLRP3, caspase-1/11, and RIPK3/caspase-8.

K⁺ and Cl⁻ efflux, ROS, and Ca²⁺ influx are increased by MtbΔpknF infection.

Three isoforms of Chinook salmon PKR are present in CHSE-EC cells.

Full-length PKR triggers apoptosis and inhibits de novo protein synthesis.

Endogenous PKR is not involved in translational arrest during VHSV infection.

Conformational changes occur in C1s surface loops upon complexing with C1-INH.

Residues outside of the C1-INH reactive center loop are important for C1s recognition.

C1s exosites are not conserved between C4 and C1-INH.

Grass carp IgM⁺ plasma cells (PCs) exhibit robust phagocytic ability.

Phagocytic IgM⁺ PCs can secrete antigen-specific IgM.

All teleost IgM⁺ PCs have phagocytic potential.

IRF10 and IRF11 regulate type I IFN expression synergistically in zebrafish.

The structures of IRF10-DBD-DNA, IRF11-DBD-DNA, and IRF11-DBD-apo were determined.

IRF10 functions as a controlling factor for IRF11 by competitive binding of the ISREs.

ICOS costimulation is required for both protumor Treg cell and antitumor effector T cell responses.

A Treg cell–compromised tumor environment is more permissive to Eomes-driven CTL maturation.