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Regulatory T cells (Treg cells) can destabilize in inflammatory environments. Sumida et al. show that β-catenin signaling perturbs Treg cell function in patients with multiple sclerosis and under experimental high-salt conditions.
LAG-3 is a co-inhibitory receptor on T cells, but its mode of action is controversial. Okazaki and colleagues demonstrate that LAG-3 preferentially binds stable MHC class II complexes and thereby selectively maintains tolerance of self-reactive T cells.
Immunity to one serotype of dengue virus can worsen disease following exposure to another serotype, a process called ‘antibody-dependent enhancement’. Grimes and colleagues characterize the function and structural basis of an unusual, potent and broadly neutralizing antibody that lacks such activity.
The transcription factor Pax5 enforces B cell identity. Nutt, Allan and colleagues show that Pax5 is needed to establish and maintain the three-dimensional genome organization of B cells throughout their lineage development.
PRMT arginine methyltransferases mediate post-translational modification. Takayanagi and colleagues show that a lack of PRMT5 in cells of the T cell lineage compromises their response to cytokines dependent on the common γ-chain, due to aberrant splicing of mRNA transcripts encoding the common γ-chain and its associated kinase JAK3.
Fibrin deposition occurs after the blood–brain barrier is breached. Akassoglou and colleagues generate a therapeutic monoclonal antibody that targets a cryptic fibrin epitope to suppress activation of innate immune responses in the CNS and diminish neuroinflammation.
Neutrophils are linked to tumor progression. Gabrilovich and colleagues demonstrate that neutrophils have tumor-stage-dependent alterations in motility, function and metabolism: in early phases, they are highly motile with altered metabolism, whereas at later stages, they become highly suppressive.
The kinase NIK activates a noncanonical NF-κB2 signaling pathway. Shao-Cong Sun and colleagues show that conditional loss of NIK in dendritic cells alters gut microbiome composition and TH17 cell responses, as a result of reduced expression of IL-23, pIgR and fecal IgA transcytosis.
Kubes and colleagues describe the presence in females of estrogen-driven, innate antibodies against specific oligosaccharides in EPEC that are maternally transferrable to offspring in mice and humans.
Environmental cues instruct cell fate during hematopoiesis. Igarashi and colleagues show that the transcription factors Bach1 and Bach2 promote erythropoiesis and suppress myelopoiesis. Infection and inflammatory signals suppress Bach expression, which results in anemia.
lncRNAs can regulate immune responses at a number of levels. Song and colleagues demonstrate that the lncRNA NKILA is expressed by tumor-associated cytotoxic T cells, and this predisposes them to activation-induced cell death and escape of tumors from immunologically mediated destruction.
Polić and colleagues show that the activating receptor NKG2D specifically sets the activation threshold for the activating receptor NCR1, providing a mechanism distinct from previously known mechanisms of NK cell education.
MicroRNAs regulate gene expression by targeting mRNAs via complementarity with seed sequences. Rudensky and colleagues provide genome-wide profiles of the microRNA miR-155 in multiple immune cell lineages and identify its cell-type effects on gene expression.
TH17 cells contribute to anti-fungal and anti-bacterial adaptive immune responses. Sallusto and colleagues show that the transcription factor c-Maf has an immunoregulatory role in directing gene expression and tissue residency in human IL-10+ TH17 cell subsets.
The receptor TLR3 is essential for effective responses to herpes simplex virus type 1. Miyake and colleagues demonstrate that a neuron- and astrocyte-intrinsic pathway of TLR3 and the metabolic checkpoint kinase complex mTORC2 is needed to prevent fulminant infection with this virus and encephalitis.
Locksley et al. show tissue-specific imprinting dictates the activating receptors ILC2s express, even in germ-free mice. Skin ILC2s are preferentially activated by IL-18, and IL-18 contributes to inflammation in a mouse model of atopic dermatitis.
Ugolini and colleagues show that glucocorticoid signaling induces expression of the checkpoint receptor PD-1 on NK cells to control immunopathology in a tissue-specific way.
Primary immunodeficiency can predispose patients to mycobacterial disease. Casanova and colleagues identify novel human mutations in the enzyme SPPL2A that result in selective accumulation of CD74 in a dendritic cell subset and lead to their death and the failure to mount effective TH1 responses.
Cohesin is a chromatin-binding factor that interacts at CTCF motifs to organize chromatin looping domains. Merkenschlager and colleagues show that cohesin regulates the inducible expression of inflammatory genes in macrophages and HSPCs and in human AML.
Patients who express a hyperactive mutant of the kinase PI3K exhibit defective humoral immunity. Preite et al. show that overactive PI3K leads to defective class-switched antigen-specific responses to immunization, despite augmented germinal-center formation and reactivity to commensal microbes and self antigens.