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Effective anti-tumor immune therapy in solid tumors relies on the presence of effector T cells. Inhibition of the dipeptidylpeptidase DPP4 (CD26) enhances chemokine CXCL10–mediated infiltration of lymphocytes into the tumor parenchyma, which results in diminished tumor growth.
Deep-sequencing analyses of immunoglobulin variable-segment genes from antibody-secreting cells have allowed comparisons of conventional immunization responses to disease flares experienced by patients with systemic lupus erythematosus. Such analyses provide insight into B cell recruitment and differentiation processes yielding expanded clones that contribute to this complex autoimmune disease.
Sirtuin-1 (Sirt1), a protein deacetylase known for its multiple cellular functions, including roles in metabolism, stress response and aging, is a post-translational modulator of autoimmune regulator (Aire) in central immunotolerance.
Dendritic cell progenitors commit to a specific conventional dendritic cell fate earlier than previously thought, by initiating transcription-factor regulatory circuits unique to their subtype.
Like T cells and B cells, innate lymphoid cells (ILCs) develop from common lymphoid progenitors, but how commitment to the ILC lineage is regulated has remained unclear. The transcriptional regulator TOX is important in this process.
The anti-inflammatory molecule A20 inhibits necroptotic cell death by inhibiting ubiquitination of the kinase RIPK3 at the Lys5 residue and preventing excessive formation of the RIPK1-RIPK3 necroptotic complex.
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.