Issues

The PcG protein Cbx4 favors CTL differentiation to an effector phenotype.

Cbx4 deficiency alters CTL differentiation, increasing memory formation.

Cbx4 drives effector formation mainly through its SIM motifs.

The expression of the PBX1D splice isoform in CD4⁺ T cells is associated with SLE.

PBX1D lacks the DNA-binding domain and nuclear localization sequence in exon 6.

Loss of two Lys residues in exon 6 accelerates PBX1D degradation by the proteasome.

Lower numbers of infused TIL are associated with poor overall survival in patients.

High frequencies of CD4⁺ cells are associated with reduced expansion of TIL.

Increased expression of ETS2 or OSM is associated with reduced expansion of TIL.

CLL subset #201 displays biased features of somatic hypermutation.

Subset #201 exemplifies the role of N-glycosylation in the evolution of CLL.

A STAP-2 inhibitor, iSP2, inhibits interaction of STAP-2 with CD3ζ ITAMs.

iSP2 suppresses TCR-mediated T cell activation events.

iSP2 reduces disease severity of CD4⁺ T cell–mediated EAE.

B. thetaiotaomicron drives IL-10 via a TLR2–MyD88 pathway.

B. thetaiotaomicron–secreted outer membrane vesicles mediate its immunomodulatory function.

The B. thetaiotaomicron NQR complex coordinates outer membrane vesicle biogenesis to promote IL-10 induction.

IFN-γ and TNF-α upregulate GARP on LECs, leading to increased membrane-anchored TGF-β.

TGF-β prevents LEC MHC-II from reactivating CD4⁺ T_Ms.

LECs support the maintenance of FOXP3⁺ memory CD4 T cells.

Macrophages from BCG-trained mice lead to a reduction of B. abortus burden.

Previous BCG immunization confers protection in RAG^−/− mice against B. abortus.

BCG-trained bone marrow transfer to naive mice protects against B. abortus infection.

Fungal enolase 1 binds and activates mouse and human B cells.

Mouse and human B cells secrete Abs upon stimulation with fungal enolase 1.

Fungal enolase 1 induces human monocytes, but not B cells, to secrete IL-6.

PD-L1/BTLA axis acts as a primordial substitute of PD-L1/PD-1 in fish.

PD-L1/BTLA is exploited by E. tarda to restrain CD8⁺ T cell–mediated cytotoxicity.

Insights are given into an immune evasion strategy of pathogen via eliciting PD-L1/BTLA.

CX3CR1⁺BIRC5⁺ immune cells expand with S. mansoni and S. aureus infection.

Leukocidin-deficient S. aureus does not induce CX3CR1⁺BIRC5⁺ myeloid cells.

Deletion of BIRC5 in CX3CR1⁺ cells improves survival with S. aureus infection.

Lung scRNA-seq identified two NMSC populations and one mSC population.

NMSCs but not mSCs appear to be responsive to proinflammatory cues in the lung.

NMSCs may play a functional role in lung inflammation.

RXRα in APCs regulates intestinal immune homeostasis and colitis.

RXRα regulates the expression of proinflammatory and anti-inflammatory factors.

Pharmacological activation of the RXRα pathway alleviates colitis severity in mice.

ISG65 from Trypanosoma brucei stimulates factor I degradation of complement C3b.

ISG65 forms a ternary complex with iC3b and the CR3 ligand binding domain.

ISG65 is a cross-reactive specific inhibitor of the complement alternative pathway.

TIPE1 deficiency in resident cells promotes inflammation but not colon tumorigenesis.

TIPE1 integrates the multifaceted effects of TNF-α signaling to regulate the IEC response.

TIPE and TIPE1 play redundant roles in maintaining intestinal homeostasis in mice.

IFN-γR signaling inhibits Treg expansion and peripheral Treg induction.

Impairing the IFN-γR signal in Tcons could mitigate GVHD while preserving GVL effects.

IL-27 gene therapy induces Stat3-mediated expansion of CD11b⁺Gr1⁺ myeloid cells.

IL-27 induces expansion of LSK stem cells and granulocyte–macrophage progenitor cells in bone marrow.

IL-27 gene therapy induces accumulation of M1 macrophages in tumors.