Volume 202, Issue 9, May 2019

TLR7-driven lupus-like disease is ameliorated in the absence of BCAP.

BCAP promotes TLR7/9-induced IFNα, but not IL-6, in pDC.

BCAP associates with DOCK2 and promotes CpG DNA-induced Rac1 and IKKα activation.

BCR ligation induces ROS production in two phases.

ROS production in the late phase is essential for B cell proliferation and survival.

ROS production in the late phase is mediated by NADPH oxidases, especially NOX3.

High DM overcomes poor DM/DQ2 interaction to inhibit DQ2 presentation of gliadin.

Relative low strength of gliadin peptide-DQ2 binding contributes when DM is high.

In contrast, abundant DM promotes DQ2 presentation of DM-resistant viral Ag.

TSHR A-subunit NOD.H2^h4 mice spontaneously develop pathogenic TSHR Abs.

TSHR + ITE + A-subunit nanoparticles accelerated pathogenic TSHR Ab development.

TSHR A-subunit stimulation is required to generate pathogenic TSHR Abs.

The proportion of CD14^hiCD16⁻ monocytes was increased in AP patients.

CD14^hiCD16⁻ monocyte proportions, together with their HLA-DR level, could predict AP severity.

We found that epidermal keratinocytes expressed CCK octapeptide.

CCK octapeptide expression was markedly decreased in acanthotic lesions of psoriasis.

CCK may exert a self-regulatory effect on psoriatic inflammation.

Batf3-lineage cDC1 are required for peripheral CD8⁺ T cell deletion.

The absence of cDC1 does not increase CD8⁺ T cell autoreactivity or alter the TCR repertoire.

Peripheral deletion by cDC1 does not significantly contribute to CD8⁺ T cell tolerance to self.

High levels of KIR and HLA diversity are present in all seven African populations.

Although 28 novel KIR alleles were detected, all HLA class I alleles are familiar.

KIRtelA and telB are balanced in East Africa, but KIRtelA dominates in West Africa.

P. vivax DPB:DARC interaction is essential for RBC invasion.

P. vivax–exposed individuals acquire Abs that block this interaction.

Human-derived monoclonal Abs recognize a globally conserved blocking epitope.

C. neoformans transfers between macrophages in coordinated exocytosis/phagocytosis.

Opsonin receptors are used for the transfer process.

C. neoformans must be viable for the transfer process to occur.

Brucella abortus induces a STING-dependent UPR.

Bacterial c-di-GMP recognition by STING triggers B. abortus–induced UPR.

UPR blockade inhibits B. abortus replication in vitro and in vivo.

Lamina propria macrophages are short-lived and destroyed after SIV infection.

Intestinal submucosa macrophages are long-lived and may become SIV/HIV reservoirs.

Gut biopsies are insufficient for monitoring submucosal long-lived macrophages.

AB therapy in PD patients ablated P. gingivalis from oral and hematogenous reservoirs.

This reduced inflammatory blood mDCs and IL-1R expression on Tregs in PD patients.

A favorable clinical response was related to P. gingivalis ablation and a decrease in Treg→Th17.

Critical structural elements are identified in MCT-2 that mediate FPR2 activation.

MCT-2 polymorphic variants activate human neutrophils with different potency.

Skin wounding promotes Mo expansion in mouse bone marrow.

IL-1R1 signaling is not involved in skin wounding–induced Mo expansion.

Acute gout patients express higher level of leptin and leptin receptor.

Leptin promotes MSU-induced inflammation in human and murine models of acute gout.

Leptin-exacerbating inflammation in acute gout is mediated by mTORC1 signaling.

DMF suppresses cytokine production in pDCs.

DMF blocks Myddosome formation by disrupting the MyD88–IRAK4 interaction.

DMF blocks the MyD88–IRAK4 interaction by targeting C13 in IRAK4.

IMD activation in the fat body disrupts growth and energy stores.

Inhibition of IMD signaling in Drosophila disrupts metabolic homeostasis.

Insulin mutant flies have varied responses to bacterial infection.

In a murine model of lung fibrosis, an ontogeny of inflammatory events was defined.

Mutant Sftpc^I73T expression caused early lung injury marked by a polycellular alveolitis.

Depletion of peripheral monocytes was protective from Sftpc^I73T injury.

Ly-6Clo and Ly-6Chi monocytes/macrophages have unique roles in acute HILI.

Ly-6C^lo monocytes/macrophages adopt proinflammatory phenotypes in CD11b-DTR⁺ mice.

Intranasal IFN-γ rescues CD11b-DTR+ mice from severe HILI.

The mouse α4/β1 integrin is important in the binding of IgG3 Abs to macrophages.

Phagocytosis mediated by mIgG3 Abs depends on the α4/β1 integrin.

The α4/β1 integrin is a new receptor and/or part of a receptor complex for IgG3.