Volume 203, Issue 11, December 2019

TCR signal strength regulates acetyl-CoA metabolism.

Weak TCR signals promote phosphorylation of citrate synthase via Akt.

TCR signal strength differentially regulates acetyl-lysine containing proteins.

LARI inhibits allergic reactivity while displaying an excellent safety profile.

LARI blunts allergic responses via multiple mechanisms at multiple steps.

Autoreactive T cells drive the lethal disease in Malt1PD mice.

Malt1PD mice display B cell hyperactivation to environmental Ags.

IPEX-like disease occurs in Malt1PD mice despite in vitro Treg suppressive activity.

CREMα induces DUSP4 phosphatase expression in CD4⁺ T cells.

DUSP4 promotes IL-17A and reduces IL-2 production by effector T cells.

The CREMα/DUSP4 axis is involved in the pathophysiology of SLE.

CD11c⁺ ABCs exhibit functional characteristics of MBCs.

ABCs express polyreactive B cell receptors binding diverse self-antigens.

Adoptively transferred ABCs contribute to rapid recall responses to viral Ags.

UBASH3A interacts with the TCR–CD3 complex and regulates its turnover.

UBASH3A facilitates the downmodulation of cell-surface TCR–CD3 upon TCR engagement.

UBASH3A binds to CBL-B, another T1D-associated protein that inhibits T cell function.

TNF-Tg mice develop NSIP-like lung disease with increased cDC2 and macrophages.

Anti-TNF therapy modulates prefibrotic ILD in TNF-Tg mice.

Regulatory T cells can undergo extensive intravascular crawling in skin vessels.

Mechanisms of regulatory T cell transmigration can be modulated dynamically.

RELMα (hResistin) activates pulmonary macrophages in PAH patients and hypoxic mice.

RELMα (hResistin) induces HMGB1 acetylation by suppressing Sirt1 in macrophages.

The RELMα–HMGB1 axis causes macrophage-mediated PASMC proliferation.

TLR2 directly regulates the anti-CD3–activated CD8⁺ T cells independently on APCs.

Bioenergy metabolism is important for TLR2-mediated enhancement of CD8⁺ T cells.

TLR2 enhances the antiviral CD8⁺ T cell response and the efficacy of HBV vaccine.

MHCII molecule upregulation is not required for the development of skin moDCs.

Skin CD206⁺ moDCs do not migrate to LNs in the absence of MHCII ubiquitination.

GM-CSF restores the migration of skin moDCs by upregulating CCR7 and IRF4.

Fnip1 is required for pre–B cell development/survival independent of p53 and Bcl-x_L.

Fnip1 is required for optimal inhibition of mTORC1 in response to amino acid restriction.

Fnip1 regulates TFE3 nuclear translocation and lysosome biogenesis in pre–B cells.

Two lamprey BCMA-like receptors interact with a single lamprey BAFF protein.

BCMAL1 and BCMAL2 genes are differentially expressed during VLRB cell stimulation.

BAFF-based mechanisms for B cell regulation appeared early in vertebrate evolution.

MAIT cells comprise half the CD8 T cell IFN-γ response to BCG in blood.

Frequencies of MAIT cells were not sustainably modulated by BCG vaccination.

Innate cytokines mediate BCG-induced MAIT cell responses in whole blood.

Anti–IL-15 depletes NK cells and disrupts T_EM homeostasis in SIV-infected RM.

IL-15 inhibition does not alter SIV replication dynamics or CD4⁺ T cell depletion.

IL-15 inhibition does accelerate reactivation of an oncogenic γ-herpesvirus.

NK cells are required for immune control of secondary T. gondii infection.

NK cells do not develop intrinsic memory-like features during T. gondii infection.

Secondary NK cell responses depend upon IL-12 and IL-23.

FOH promotes CD1d expression in human DC via activation of PPARγ, RARα, and p38 MAPK.

FOH modulates cytokine release through nuclear receptors, MAPK, and NF-κB pathways.

FOH diminishes human DC capacity to activate iNKT, Th1, and FOXP3⁺ regulatory T cells.

DR3 is highly expressed on human MAIT cells.

DR3 ligand TL1A licenses innate TNF-α production and boosts polyfunctionality.

TL1A equally augments TCR-dependent MAIT cell effector functions.

Early monocyte infiltration causes long-term microgliosis in sepsis.

Brain microglia self-proliferate during severe sepsis.

Microglia proliferation is associated with local M-CSF.

GSK3β interacts with Src tyrosine kinase.

Src positively regulates antiviral immune response.

Src undergoes K63-linked ubiquitination by TRAF2.

Pseudomonas bacterial lung infection leads to pulmonary ACE2 dynamic variation.

The ACE2 dynamic alteration is critical in regulating neutrophilic lung inflammation.

ACE2 modulates IL-17–mediated neutrophil influx by impacting STAT3 activity.

Exercise enhances resolution of acute inflammation and RvD1 biosynthesis.

Epinephrine stimulates macrophage production of RvD1 through α1-AR.

α1-AR blockade in vivo abrogates exercise-enhanced resolution.

Ubc9 interacts with and SUMOylates the immune adaptor SLP-76 in T cells.

Synergy of SLP-76–Ubc9 on IL-2 transcription is SLP-76 SUMOylation dependent.

SLP-76 SUMOylation is required for Ubc9-NFAT complex assembly for IL-2 transcription.

Recognition of monomeric Le^x by 1G5F6 using a panel of Le^x analogues was studied.

Anti-Le^x mAbs bind in different ways; the hydrophobic patch of β-d-Gal is essential.

Uhrf1-mediated DNA methylation represses Tnf-α expression in macrophages.

Uhrf1 deficiency augments Tnf-α expression, resulting in aggravated colitis.

Tnf-α triggers macrophage activation through destabilizing Uhrf1 protein.

A mucosally associated lymphoid tissue is identified in teleost pharyngeal cavity.

Trout pharyngeal bacteria are mainly coated with secretory IgT.

Teleost IgT plays a vital role in protecting the PC from invading pathogens.

Inhibitory receptors are upregulated on peripheral Tregs of DC-deficient mice.

Tregs from DC-deficient mice are functionally impaired.

Tregs require DCs for inhibition of T cell transfer-induced colitis.

STAT3 induces the expression of Wnt5a in CLL cells.

Wnt5a provides CLL cells with survival advantage.