Volume 204, Issue 3, February 2020

PcnAMP is processed by endogenous trypsin into the short active form.

PcnAMP destroys the bacterial cell membrane integrity in vitro.

PcnAMP is important in host resistance to Aeromonas hydrophila infection.

All populations of foreign Ag-specific B cells cross-react with self-antigens.

Moderate cross-reactivity to self-antigen promotes optimal naive B cell response.

Twelve-hour cDC1 IL-27p28 expression predicts adjuvant-elicited CD8 T cell memory.

cDC1 IL-27p28 expression uniquely stratifies T cell–inducing adjuvants.

BAFF-silenced DCs exhibited an immature and tolerogenic phenotype.

BAFF-silenced DCs alleviated mouse CIA by modulating the Th17/Treg balance.

BAFF might be a promising genetic target to generate tolDCs for RA treatment.

IL-9R^−/− mice develop severe EAE with increased frequency of GM-CSF⁺ CD4⁺ T cells.

IL-9R^−/− DCs induce GM-CSF in CD4⁺ T cells and contribute to disease worsening.

HIV-specific T cell responses persist despite long-term viral suppression.

Timing of ART initiation impacts the quality of the HIV-specific T cell responses.

Baseline PBMC transcriptome is different in HIV-infected children treated early.

IL-5 regulates development in BM and accumulation of eosinophils in the lung.

IL-13 induces airway eosinophilia, AHR, and goblet cell metaplasia.

Development and transmigration of eosinophils are synergistically affected by both cytokines.

The P2X7 receptor requires Eros as a chaperone to be expressed at plasma membrane.

The ATP-triggered IL-1β secretion in macrophages is strongly reduced without Eros.

T cell signals trigger activation of multiple events in the teleost Ca²⁺–NFAT axis.

Tight regulation of Ca²⁺–NFAT is pivotal for teleost T cell activation and function.

Ca²⁺–NFAT is a primitive regulatory strategy that emerged in teleost T cells.

Kidney CD4 T cells significantly increase Lcn2/NGAL expression following IR injury.

CD4 T cell Lcn2/NGAL protects against IR-induced AKI.

Lcn2 expression increased in ischemic CD4 T cells from human kidney.

L. donovani induces SOCS1 in BMMфs by PI3K/Akt/Egr2 and IDO/kynurenine pathway.

PGE2 from infected BMMфs activates cAMP/PKA-mediated SOCS3 expression in T cells.

This inhibited STAT1- and STAT4-mediated IFN-γ and IL-12 synthesis in immune cells.

Novel TLR triagonist platforms have adjuvant activity in vivo.

The TLR triagonist adjuvants tune immune responses to subunit vaccination.

Enhanced Ag cross-presentation by naringenin is due to moderate ROS induction.

Naringenin potentially facilitates therapeutic vaccines against cancers or viruses.

Flavonoids manipulate intracellular ROS, making them excellent immunomodulators.

Brucella decreased TXNIP to promote its intracellular growth in macrophages.

Reduced TXNIP promotes Brucella intracellular growth via reduction of NO and ROS.

The expression of iNOS and the production of NO were dependent on the Brucella T4SS.

IL-10 is not detrimental to early M. tuberculosis infection outcome.

Lack of IL-10 influences immune responses and fibrosis in granulomas.

Modeling predicts that prolonged lack of IL-10 leads to improved infection outcomes.

Neutrophils produce high levels of Cxcl2 in response to whole bacteria.

Cxcl2 production depends on sensing of bacterial nucleic acids by TLR7, 9, and 13.

Cxcl2 acts autocrinously to enhance antibacterial activities and its own production.

Mtb LAM stimulates neutrophil cytokine production via TLR2/1 signaling.

Mtb LAM–elicited neutrophil responses are distinct from the TLR2/1 agonist Pam₃CSK₄.

Eosinophilia is a characteristic feature of allergic airway inflammation and asthma.

TrkA activation by eotaxin-1 promotes eosinophil migration and airway inflammation.

Inhibiting TrkA kinase mitigates airway eosinophilia and suppresses a Th2 phenotype.

dsRNA induces an intrauterine antiviral response in early pregnancy.

The antiviral response reduces imprinted gene expression and fetal–placental size.

Type I IFNs inhibit trophoblast stem cell developmental potential.

TLR dimerization blockade impairs TLR2/1 and TLR2/6 signaling in macrophages.

TLR2 dimer blockade ameliorates acute experimentally induced colitis.

Treatment blunts monocyte activation and allows generation of tissue macrophages.

NNV-specific VLRBs were developed using a library screening system.

The binding ability of this Ab was enhanced through modular engineering.

VLRB could be an alternative neutralizing Ab against Betanodavirus infection.