Contents
08 July 2020
Vol 12, Issue 551
Vol 12, Issue 551
Research Articles
- Cyclin-dependent–like kinase 5 is required for pain signaling in human sensory neurons and mouse models
CDKL5 controls nociception in human neurons and murine models of CDKL5 deficiency disorder via CaMKII-dependent mechanisms.
- An extracorporeal bioartificial liver embedded with 3D-layered human liver progenitor-like cells relieves acute liver failure in pigs
A bioartificial liver device containing human progenitor-like cells attenuates acute damage and inflammation, enhancing liver regeneration in pigs.
- Staphylococcus Agr virulence is critical for epidermal colonization and associates with atopic dermatitis development
Skin colonization at 6 months of age by S. aureus with functional Agr quorum sensing associates with later atopic dermatitis development in infants.
- Gut microbiota dysbiosis and altered tryptophan catabolism contribute to autoimmunity in lupus-susceptible mice
Gut microbiota dysbiosis induces lupus-like autoimmunity in mice through altered tryptophan catabolism.
- PRMT5 control of cGAS/STING and NLRC5 pathways defines melanoma response to antitumor immunity
PRMT5 expression in melanoma suppresses inflammation and antigen presentation, suggesting that its inhibition could potentiate immunotherapy.
Editors' Choice
- Clearing the path for gene therapy
Degrading antibodies allows gene transfer in the presence of anti-AAV antibodies.
- Do dendritic cells hold the key to regulating cancer antitumor immunity?
PD-L1 blockage on dendritic cells, but not macrophages, may enhance antitumor or CD8+ T cell responses leading to greater tumor growth inhibition.
- Paving the path to inpatient printing
3D bioprinting in situ in various tissues in a live animal enables in vivo confined cell delivery.
About The Cover
ONLINE COVER Painful Deficiency. This image shows epidermal innervation in a patient with CDKL5 deficiency disorder (CDD), an X-linked disorder characterized by developmental epileptic encephalopathy. To better understand the disease phenotype, La Montanara et al. studied patients with CDD and noted alterations in pain perception. The authors showed that CDKL5 is expressed in sensory neurons and controls nociception. In rodents, Cdkl5 deletion reduced pain sensitivity by modulating calcium-dependent TRPV1 signaling. Pain perception assessment and restoration should be considered for patients with CDD. [CREDIT: J. CLARK, B. HARRISON/UNIVERSITY OF NEW ENGLAND; P. LA MONTANARA/IMPERIAL COLLEGE LONDON]
