Issues

Tal1 limits the number of ST-HSC priming lymphoid genes.

Tal1 limits the number of Rag2-GFP⁺ LMPPs.

Tal1 restrains the frequency of T lymphocyte–biased LMPPs.

CLP-induced polymicrobial sepsis has the capacity to attenuate tumor growth.

Sepsis reinvigorates tumor-infiltrating CD8 T cells.

Checkpoint blockade after sepsis further improves survival of tumor-bearing hosts.

Proteomics analysis shows the upstream proline signature of HLA class I ligands.

Proline at upstream positions 1–3 attenuates CTL responses to a downstream epitope.

The finding contributes to prediction of naturally presented CTL epitopes.

Trogocytosis-mediated signaling promotes IL-4 expression and T_H2 differentiation.

T_H2 cells perform trogocytosis more efficiently than T_H1 or nonpolarized cells.

In vivo–generated, trogocytosis-positive cells are predominantly T_H2.

The covalent BTK inhibitor evobrutinib blocks B cell and myeloid cell activation.

Evobrutinib is efficacious in mouse models for RA, SLE, and cutaneous anaphylaxis.

Covalent binding allows modeling the relationship between BTK occupancy and efficacy.

Nur77 expression correlates with the degree of autoreactivity of individual B cells.

Nur77 is dispensable for receptor editing, central deletion, and anergy.

Nur77 restrains the survival of mature self-reactive B cells.

TLR9-primed human B-CLL clones respond to IL-15 with AKT and STAT5 activation.

PI3K/AKT and STAT5 pathways elevate cyclin D2 and repress ATM, TP53BP1, and MDC1.

Inhibitors of PI3K or STAT5 block in vitro B-CLL cycling induced by CpG DNA and IL-15.

The pharmacological activity of Imprime is dependent on naturally occurring serum ABA.

A threshold of IgG ABA is necessary for Imprime-mediated innate immune responses.

It is likely that high-ABA subjects will be more prone to infusion-related reactions.

The otubain YOD1 fine-tunes MAVS-RLR pathway–mediated antiviral immunity.

YOD1 interacts with MAVS on mitochondria.

YOD1 deubiquitinates MAVS and abrogates aggregation of MAVS.

Arf6 partially colocalized with PLD1 on vesicles and with PLD2 at the plasma membrane.

Active Arf6 is recruited to nascent phagosomes.

Arf6 regulates PLD activity and PA synthesis during phagocytosis.

Myeloid-specific conditional deletion of BVR-A results in increased response to LPS.

Macrophages isolated from LysM-Cre:BVR^fl/fl showed elevated levels of C5aR1.

Deletion of BVR-A resulted in enhanced macrophage chemotaxis toward C5a.

BVR-A–modulated chemotaxis and RANTES levels are dependent in part on C5aR1.

Bach2 deletion in CD4⁺ T cells results in preferential Tfh cell differentiation.

The CXCR5 induction in the absence of Bach2 occurs before the upregulation of Ascl2.

Bach2 is critical for CD4⁺ T cell memory, including Tfh cell memory.

LCs express LIGHT, and chimeras lacking LIGHT in LCs have reduced skin DC migration.

Lymphatic endothelial cell–specific LTβR is required for skin DC migration.

LIGHT-LTβR signaling axis activates lymphatic endothelial CCL21/CCL19 expression.

Malt1 is required for the development and function of Treg cells.

Malt1 protease activity in Treg cells could be a target for tumor therapy.

Traumatic injury alone without infection can induce emergency hematopoiesis.

Trauma induces emergency hematopoiesis through IL-1 -dependent production of G-CSF.

ZIP requires GM-CSF and IRF4 signaling.

The ZIP macrophage phenotype is altered by a lack of GM-CSF or IRF4.

GM-CSF–IRF4 signaling upregulated MHCII expression in ZIP macrophages.

ZIP is independent of CCL17.

TLR2 plays a key role in gut serotonin production by both resident microbiota and a parasite.

TLR2 in nonhematopoietic cells is largely responsible for serotonin production in the gut.

We show TLR2 signaling–based novel mechanism of serotonin production in the gut.

MyD88 deficiency in donor Tcons with Tregs protected against alloreactivity and aGVHD.

This protective effect uses ST2 but not the IL-1R or TLR4 pathways.

PR interacts with STAT1 in breast cancer cells.

PR attenuates IFN-induced STAT1 phosphorylation in breast cancer.

IFN signaling via STAT1 is more robust in breast cancer cells lacking PR.

Losartan blocks CCL2–CCR2 monocyte recruitment to suppress lung metastasis growth.

Losartan functionally antagonizes CCL2–CCR2 ERK activation, independent of its AT1R target.