Issues

TAK1 protects macrophages from proinflammatory cell death in TLR and TNFRI signaling.

The cell death machinery is dependent on active caspases and GSDMD processing.

TAK1 in macrophages both positively and negatively controls host inflammatory responses.

A bicistronic dual-reporter mouse enables visualization of allelic CXCR3 expression.

CXCR3 escapes X chromosome inactivation (XCI) in T cells in vivo during infection.

XCI escape by CXCR3 potentially contributes to enhanced Th1 responses in females.

Citrullination in macrophages is induced during pyroptosis.

The NLRP3 inflammasome is regulated by Ca²⁺-dependent PAD enzymes.

Tcf1-mediated repression of Blimp1 is functionally critical for T_FH differentiation.

An intron-3 regulatory region in the Blimp1 gene is necessary for optimal T_FH response.

BCG immunization alters the cell types targeted for early M. tuberculosis infection.

Vaccine-induced CD4 T cells are required for this transfer of infection.

T cell activation within the lung first occurs distal to sites of infection.

Lone star tick proteins induce IgE production and hypersensitivity reactions in mice.

CD4⁺ T cell help is required for both sensitization and recall IgE production.

MyD88 deficiency in B cells disrupts IgE production.

Injection of allogeneic Ag-loaded EVs significantly increases IgG in mice.

Two injections of syngeneic or allogeneic EVs result in long-term immunity.

Syngeneic and allogeneic EVs are equally potent in inhibiting tumor growth.

We studied whether and to what extent IFN-α causes SLE.

We found that increase of IFN-α alone was sufficient to cause SLE.

The DNT cells as expanded by IFN-α directly caused organ manifestation of SLE.

PD-1 blockade or deficiency unleashes follicular insulin-specific CD4⁺ T and B cells.

PD-1 limits T follicular helper cell survival in the germinal center.

PD-1 blockade increases insulin autoantibody production in diabetes-prone mice.

Cholesterol crystals induce coagulation through monocyte TF.

Monocyte TF induction is blocked by complement inhibitors to C3, C5, or C5aR1.

Monocyte TF induction is dependent on complement C5aR1.

COX-1 deficiency impaired T_FH cell development during influenza infection and KLH immunization.

COX-1–derived metabolite PGE₂ and its receptors EP2/EP4 mediate the effect of COX-1 on T_FH cells.

TRIM29 is induced in NK cells and inhibits NK functions.

TRIM29 deletion in NK cells enhances IFN-γ production.

TRIM29 ubiquitinates and degrades TAB2 in activated NK cells.

In vivo administration of a peptide can promote T cell selection in the thymus.

Affinity for TCR/pMHC during positive selection fine-tunes peripheral T cells.

MS-associated SNP rs17066096 influences IL-22BP levels.

IL-22BP promotes neuroinflammation by blocking IL-22 signaling.

IL-22 reduces T cell IFN-γ production.

KMO inhibition improved clinical outcomes of CD4⁺ T cell counts and body weight.

KMO inhibition increased naive T cell frequency and lowered PD-1 expression.

TLR ligands induce IL-26 secretion from PBMCs in an IL-1β–dependent manner.

IL-1β induces rapid IL-26 release by IL-1RI⁺ Th17 cells without TCR activation.

IL-1β–stimulated T cells mediate an antimicrobial activity via IL-26.

IL-36γ conferred MDMs M. tuberculosis resistance through activation of autophagy.

IL-36γ induced autophagy relying on WNT5A/COX-2/AKT/mTOR axis.

IL-36γ may be a potential candidate for immune therapy of tuberculosis.

Low affinity–stimulated CD8⁺ T cells have an advantage in forming T_RM.

High and low affinity–stimulated T_RM have distinct transcriptomes.

T_RM longevity is not impacted by strength of TCR stimulation.

CD69 is not required for the establishment of CD8⁺ T_RM in every nonlymphoid tissue.

In the kidney, CD69 is required for CD8⁺ T_RM regardless of immunization approach.

CD69 deficiency prevents generation of KLF2^low T_RM in the kidney.

Adiponectin KO mice show increased pathology in a mouse model of IA.

KO mice show increased inflammatory and decreased anti-inflammatory phenotypes.

Increased lung inflammation in KO mice is independent of invasive fungal growth.

Deficiency of NK cells leads to enhanced susceptibility to T. congolense infection.

NK cells mediate protection during T. congolense infection via perforin.

We describe a naive-like M. tuberculosis–specific CD4⁺ IFN-γ⁺ memory T cell (T_NLM).

T_NLM provide protection equal to known memory subsets against M. tuberculosis lung infection.

KLF12 deficiency does not affect NK cell development and effector functions.

KLF12-deficient NK cells have increased expression of Btg3 and the IL-21 receptor.

IL-21 induced Btg3 and inhibited KLF12-deficient NK cell proliferation.

NAFLD microenvironments increase Tim-4 expression in macrophages.

Tim-4 in macrophages suppresses NLRP3 inflammasome depending on PS binding motif.

Tim-4 promotes phosphorylation of AMPKα by interacting with LKB1.

NAC1 enhances the virus-induced IFN signaling and activation of TBK1 and IRF3.

NAC1 inhibits the replication of RNA viruses.

NAC1 promotes the recruitment of TBK1 to MAVS upon viral infection.

FBXO6 can negatively regulate the activation of IFN-I signaling.

FBXO6 interacts with and mediates IRF3 degradation independent of SCF complex.

AZM’s immunomodulatory mechanism involves both NF-κB and STAT1 pathways.

AZM’s impact on STAT1 phosphorylation works in part through IKKβ.

V-ATPase is required for ERK-mediated 15-LOX-1 expression during M2 polarization.

Inhibition of V-ATPase prevents 15-LOX-1–mediated SPM biosynthesis in M2 macrophages.

Targeting V-ATPase delays resolution in murine peritonitis with decreased SPM levels.

Early T-BET expression is important for early acquisition of CD8⁺ T cell lineage–specific function.

T-BET expression shuts down inappropriate T cell lineage functions in activated CD8⁺ T cells.

Early T-BET expression is required for activation of specific IFN-γ transcriptional enhancers.

The interactomes of CD2 and CD28 were identified.

CSK is a specific and direct interactor of activated CD28.

CSK regulates signaling downstream of CD28.

Neutrophil proteomes are mapped during homeostasis or following lethal PR8 infection.

ISGs are first elevated in BM and then BAL neutrophils following lethal PR8 infection.

BAL neutrophil proteomes exhibit a modest capacity for pathogen tuning.

LILRB1 inhibits BiTE molecule–induced cytolytic activity of human CD8⁺ T cells.

LILRB1 and PD1 express on distinct human CD8⁺ T cell subsets in tumors.

LILRB1 and PD1 blockades have synergistic effects to enhance CD8⁺ T cell activity.