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Due to their role in regulating DNA-methylation patterns, the TET proteins, in particular TET2, have emerged as key participants in tumorigenesis. Now the spotlight shifts to TET1 and its role as a tumor suppressor in lymphomagenesis.
The mediobasal hypothalamus detects increased amounts of tumor necrosis factor during the early phases of inflammation and relays this information to cells of the adaptive immune system by mobilizing free fatty acids.
The cell-surface receptor TREML4 amplifies cellular responses to single-stranded RNA by regulating recruitment of the adaptor MyD88 to the receptor TLR7. Mice lacking TREML4 show impaired antiviral immunity but also reduced severity of lupus-like disease.
The methyltransferase Ezh2, an epigenetic regulator associated with tumor-cell metastasis, also methlyates the cytoplasmic integrin adaptor talin. This modification inhibits the binding of talin to F-actin, which enhances the migration and invasion of dendritic cells and neutrophils.
Guanylate-binding proteins (GBPs) induced by type I interferon signaling cause lysis of Francisella bacteria that have reached the host-cell cytosol. The liberated bacterial DNA is then sensed by the cytosolic AIM2 inflammasome, which activates caspase-1 and leads to pyroptotic cell death.
Stromal cells in the subcapsular sinus of the lymph node 'decide' which cells and molecules are allowed access to the deeper parenchyma. The glycoprotein PLVAP is a crucial component of this selector function.
Interleukin 7 (IL-7) promotes the self-renewing ability of CD4− CD8− double-negative thymocytes by both supporting cell growth and repressing rearrangements of the locus encoding the T cell antigen receptor (TCR).
The transcription factor Sox2 has an additional function in neutrophils, as a cytoplasmic sensor of DNA. Upon binding bacterial DNA, Sox2 initiates a signaling cascade dependent on the kinase TAK1 and adaptor TAB2 that culminates in the expression of genes encoding pro-inflammatory molecules.
Sequencing studies have provided a comprehensive catalog of the expression of intergenic long noncoding RNAs (lincRNAs) in 13 subsets of human T cells and B cells. Subtype-selective lincRNAs are among those identified, including linc-MAF-4, that might regulate T cell differentiation.
Direct antagonism between interleukin1 (IL-1) and the vitamin A metabolite retinoic acid tips the balance between differentiation into the TH17 subset of helper T cells or into regulatory T cells by influencing the transcription factors STAT3 and STAT5.
Genome-wide transcriptional profiling of tissue-resident innate lymphoid cells (ILCs) has provided important insight not only into their developmental relationships and phenotypic plasticity but also into previously unknown functions.
Optimal immunosuppression by regulatory T cells (Treg cells) relies on gene-expression and signaling modules that are customized to the target cell. The kinase CK2 is upregulated in Treg cells and controls a newly identified Treg cell subset that acts on dendritic cells to suppress T helper type 2 inflammatory responses in the lungs.
Type 2 cytokine–producing innate lymphoid cells (ILC2 cells) can respond to interleukins IL-25 and IL-33. Distinct subsets are now recognized as inflammatory ILC2 cells and natural ILC2 cells that differ in their responses to these cytokines.
Regulatory T cells require the phosphatase PTEN to maintain suppressive function in homeostatic conditions through preserved expression of CD25 and the transcription factor Foxp3.
The chemoattractant receptor GPR15 directs the homing of T cells to the colon; however, GRP15 expression differs in the effector and regulatory T cell subsets of humans versus those of mice. These findings have profound implications for the potential targeting of GRP15 for therapeutic intervention.
The identification of a new class of cross-reactive monoclonal antibodies that strongly neutralize all four serotypes of dengue virus has important implications for vaccine design as well as for the evaluation of vaccines and of natural infection with dengue virus.
Ligation of the Toll-like receptor TLR7 in human CD4+ T cells elicits an anergic state that may contribute to CD4+ T cell hyporesponsiveness after infection with human immunodeficiency virus type 1 and may also enhance propagation of this virus.
Virus-triggered type I interferon induces the lysine methyltransferase Setdb2; this then generates repressive histone marks on the promoters of genes encoding molecules important for antibacterial immunity. This process can contribute to influenza virus–associated bacterial superinfection.
T cells with increased self-reactivity and marked by high expression of the negative regulator CD5 differ in gene-expression patterns and are poised for greater bursts of proliferation when they encounter foreign antigens.
