Volume 204, Issue 4, February 2020

Constitutive IL-6 overproduction promotes myeloid cell–driven inflammation.

IL-6Rα (CD126) is indispensable for IL-6–mediated STAT3 activation in mice.

Allergin-1 inhibits HDM-induced Syk activation via SHP-1 in CD11b⁺ DC.

Allergin-1 suppresses Th2 response by inhibiting Syk-mediated PGE₂ production in DC.

A small molecular activator of PKM2 attenuates allergic airways disease in mice.

Activation of PKM2 decreases IL-1β–induced airway inflammation.

PKM2 activation decreases IL-1β–induced nuclear phosphorylation of STAT3.

ICD of CT26 cells relies mainly on AH1 tumor Ag expression.

AH1-deficient necroptosis remains more immunogenic compared with apoptosis.

Necroptotic, but not apoptotic, CT26 cells generate immunity against neoepitopes.

Anticancer VR23 also effectively downregulates inflammatory cytokines in monocytes.

VR23 effectively downregulates MCP-1, IL-6, and cell migration in human synoviocytes.

VR23 effectively downregulates lung inflammation caused by LPS in mice.

IFN-γ but not type I IFN signaling is indispensable for TLR7-driven autoimmunity.

IFN-γ promotes TLR7-accelerated SLE by regulating multiple cellular pathways.

IFN-γ signaling in B cells is required for development of TLR7-accelerated SLE.

IMP761 is a humanized IgG4 LAG-3–specific Ab with agonistic properties.

IMP761 is immunosuppressive in vitro and in vivo.

Targeting LAG-3 represents a promising novel therapeutic approach for treating AID.

Activated human Th cells show IL-3R surface expression, which is increased by IL-4.

IL-3R⁺ cells show a Th2 phenotype, and their effector functions are enhanced by IL-3.

A higher number of IL-3– and IL-3R–expressing Th cells were seen in allergic patients.

Amphioxus has IRAK4 and Pelle; Pelle was displaced by IRAK1/2/3 in vertebrates.

IRAK4 and Pelle show different function in amphioxus, vertebrates, and Drosophila.

IRAKs may confer plasticity to the evolution of the TLR/IL-1R pathways.

PI3K competes with STAT5 in IL-7R signaling and maintains an appropriate signal balance.

Early and memory T cell development is modulated by a competition between IL-7R signals.

A competition in IL-7R signaling modulates the population size of peripheral T cells.

αβ TCR sequences of tTreg and Tconv are distinguished by an ML algorithm.

A fraction of αβ TCR sequences of tTreg and Tconv are conserved across mice.

OCP express CX₃CR1 and, in unperturbed conditions, differentiate into osteoclasts.

The contribution of circulating CX₃CR1⁺ OCP to OC development is low during homeostasis.

Mature OC can originate from circulating CX₃CR1⁺ cells during fracture repair.

SP induces the HMGB1 gene in BM stroma.

NK-A, via HMGB1, negatively regulates SP effects on hematopoiesis.

Humanized mice confirmed HMGB1 exerting negative hematopoietic effects.

A new, MHC-linked class I gene (UDA) was found in cartilaginous fishes.

UDA is monomorphic and in single/low copy number in elasmobranchs.

Chondrichtyans have at least four class I lineages, one classical and three nonclassical.

Bicistronic Ag–molecular adjuvant vectors induce distinct immune profiles.

CCL20 and CCL28 induce homing of Ag-specific T cells to the female genital tract.

CCL20 and CCL25 induce homing of Ag-specific B cells to the intestinal mucosa.

Primary TBE immunization induces heterogenous magnitude of CD4⁺ T cell response.

The response is marked by IL-2, TNF, and CD154 expression after each vaccine dose.

IFN-γ response by memory CD4⁺ T cells in TBE vaccinees is lower than in TBE patients.

BHLHE40 is required for protective immunity to the helminth H. polygyrus.

BHLHE40 is required for normal T_H2 gene transcription and cytokine production.

CSF2RB-dependent cytokines can compensate for each other during type 2 immunity.

Vinpocetine suppresses S. pneumoniae–induced inflammation in vitro and in vivo.

Vinpocetine inhibits S. pneumoniae–induced inflammation via upregulating CYLD.

CYLD suppresses S. pneumoniae–induced inflammation via inhibiting ERK.

The genetic variation in the proximal promoter region alters MHCII expression.

Lower MHCII-DRB expression leads to poor parasite clearance.

MHCII gene regulation determines the immunity to malaria.

Neutrophils express LILRB3, which is released in a soluble form upon activation.

LILRB3 inhibits FcαR-mediated neutrophil activation and effector functions.

Deficiency in icIL-1Ra1 aggravates psoriasis-like skin inflammation in mice.

icIL-1Ra1 is released from keratinocytes during lytic cell death.

icIL-1Ra1 counteracts the inflammatory effects of the alarmin IL-1α.

NI in the colon affects barrier function later in life.

NI sensitizes the Mir155 promoter for aberrant epigenetic activation.

miR-155 suppresses E-cadherin protein expression in the colonic epithelium.

Angiogenesis contributes to the lung premetastatic niche in a model of breast cancer.

This angiogenesis is initiated by C5a/C5aR1-regulated MDSC.

Inhibition of C5aR1 combined with antiangiogenic vaccines reduces lung metastasis.

IL-33 treatment upregulated PGD₂ synthesis genes.

IL-33–elicited lung ILC2 accumulation was partially dependent on the PGD₂ receptor CRTH2.

CRTH2 controlled IL-33–elicited ILC2 lung accumulation via migration/tissue retention.

ARF6 regulates the polarization of RPH3A and RAB21 at the plasma membrane.

ARF6 binds to RPH3A and augments the interaction between plasma membrane PtdIns4P and RPH3A.

ARF6 is important for neutrophil adhesion on the inflamed endothelia.

Choice of cell line is critical for functional glycosylation of human IgG1-Fc.

Sialylated IgG1-Fc monomers block influenza B only when made by CHO-K1 cells.

B. thetaiotaomicron CPSs control the activation of T cells and the clearance of Ag in vivo.

Antistimulatory CPSs activate innate immunity weaker than prostimulatory CPSs.

Antistimulatory CPSs block APC access, which can be rescued by opsonization.

IRF4-expressing cDC2 promote early T cell–dependent colitis.

IRF4-expressing cDC2 promote the generation of colitogenic CD4⁺ T cells.

IRF4-expressing cDC2 are not required for Treg-mediated suppression of colitis.

MCs are mainly located in hypoxic zones of murine melanoma tumors.

Hypoxia induces CCL-2 production via ROS generation and LVDCCs activation.

Hypoxia promotes glutathionylation and membrane translocation of LVDCCs in BMMCs.