Contents
10 October 2018
Vol 10, Issue 462
Vol 10, Issue 462
Focus
- T cells take aim at a ubiquitous autoantigen in multiple sclerosis
CD4+ T cells from multiple sclerosis lesions target a ubiquitous self-antigen that is shared by gut commensal bacteria (Planas et al., this issue).
Research Articles
- GDP-l-fucose synthase is a CD4+ T cell–specific autoantigen in DRB3*02:02 patients with multiple sclerosis
GDP-l-fucose synthase is an autoantigen recognized by cerebrospinal fluid–infiltrating CD4+ T cells from HLA-DRB3* patients with multiple sclerosis.
- The mechanosensitive ion channel Piezo2 mediates sensitivity to mechanical pain in mice
Piezo2 ion channels mediate mechanical allodynia in mice.
- PIEZO2 mediates injury-induced tactile pain in mice and humans
The stretch-gated ion channel PIEZO2 is required for inflammation-induced tactile allodynia.
- ITGBL1 modulates integrin activity to promote cartilage formation and protect against arthritis
ITGBL1 promotes chondrogenesis and protects joint cartilage from osteoarthritis by inhibiting integrin-extracellular matrix interaction.
- Long noncoding RNA lnc-TSI inhibits renal fibrogenesis by negatively regulating the TGF-β/Smad3 pathway
A human long noncoding RNA targeting the TGF-β/Smad pathway reduced fibrogenesis in mouse models of renal fibrosis.
Editors' Choice
- Ironing out the mechanisms of chronic bacterial infection
Molecular evaluation reveals an important role for nutrient-dependent intracellular trafficking in chronic bacterial otitis media.
- Predicting pathology provides prostate prognostication
A live primary cell phenotypic assay with single-cell resolution can predict postsurgical adverse pathology with >80% accuracy for patients with prostate or breast cancer.
- A nano stress reliever for sepsis
A peroxide scavenger nanoparticle reduces systemic inflammation in mouse models.
About The Cover
ONLINE COVER When Feathers Become Thorns. This image represents the concept of allodynia, a sensation of pain (thorns) induced by non-painful stimulation of the skin (feather) that is triggered by inflammation or nerve injury. A molecular mechanism mediating this alteration in pain sensitivity involves the ion channel Piezo2 (Murthy et al. and Szczot et al.). Sensory neuron expression of Piezo2 was shown to be critical for the development of allodynia in animal models. Individuals with PIEZO2 loss-of-function mutations did not develop allodynia, suggesting that targeting PIEZO2 might be effective for treating this painful condition. [CREDIT: ALAN HOOFRING/NIH MEDICAL ARTS]