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DDX41, a member of the DExD/H-box helicase family, senses viral DNA and triggers type 1 interferon responses in a manner dependent on the adaptor STING, as reported by Liu and colleagues (p 959; News and Views by Barber, p 929). DDX41 mutants that lack the STING-binding DEADc domain (green dots) fail to associate with cytoplasmic STING (red); DAPI stains the nucleus (blue). Original image by Musheng Bao. Artwork by Lewis Long.
ASC has emerged as an adaptor for inflammasome sensors in cells of the innate immune response. New inflammasome-independent roles have been identified for ASC in the control of adaptive immunity; these include the post-transcriptional regulation of cytoskeletal rearrangements.
The antiviral factor APOBEC3G upregulates the expression of ligands for the activating receptor NKG2D via DNA damage induced by the viral protein Vpr in cells infected with human immunodeficiency virus. The virus overcomes greater susceptibility to natural killer cell–mediated lysis by targeting APOBEC3G for degradation.
T cell tolerance is essential to the prevention of autoimmunity. The ubiquitin E3 ligase Peli1 acts as a negative regulator of T cell activation and contributes to the maintenance of self-tolerance.
The sensing of pathogen-associated DNA in the cytoplasm is an important trigger of host-defense responses that include the production of type I interferon. A new study suggests that the DExDc helicase DDX41 may function in dendritic cells as a DNA sensor to activate STING-dependent innate immune responses.
Colonic patches and isolated lymphoid follicles are lymphoid tissues that exist in the intestine. Ouyang and colleagues show that interleukin 22 maintains these structures and contributes to gut immune defenses during infection.
The development of RORγt+ innate lymphoid cells (ILCs) remains poorly defined. Golub and colleagues define the stages of fetal and adult RORγt+ ILC maturation and show that adult RORγt+ ILCs mature outside the bone marrow, in a Notch2-dependent manner.
Sensors of cytosolic nucleic acid can detect the presence of viruses. Liu and colleagues identify the helicase DDX41 as a sensor of double-stranded DNA that initiates upregulation of type I interferon dependent on the adaptor STING in myeloid DCs.
Natural killer T cells recognize glycolipid ligands in the context of the antigen-presenting molecule CD1d. Kronenberg and colleagues show that these cells recognize ligands derived from the pathogens Streptococcus pneumonia and group B Streptococcus.
The cytidine deaminase APOBEC3G has an important intrinsic antiviral function. Collins and colleagues show that APOBEC3G can also trigger a protective natural killer cell response by damaging host DNA.
Viral microRNAs can modulate a variety of host genes. Ahn and colleagues identify a human cytomegalovirus microRNA that downregulates the peptide-processing enzyme ERAP1 and prevents presentation of antigenic viral peptides.
The transcription factor E2A and Id proteins play antagonistic roles. Murre and colleagues show Id3 expression increases after the pre-TCR checkpoint and is required to maintain the naïve T cell phenotype.
T cell activation is tightly regulated by various regulatory mechanisms. Sun and co-workers show that the ubiquitin ligase Peli1 contributes to the maintenance of peripheral T cell tolerance by negatively regulating the transcription factor c-Rel.
The adaptor ASC functions in inflammasome assembly. Kanneganti and colleagues show that ASC has an inflammasome-independent role in regulating the stability of Dock2 mRNA and thereby governs the chemotaxis and phagocytosis of cells of the immune response.