Issues

The authors describe that TLR7 and TLR8 escape X-chromosome inactivation in plasmacytoid DCs of patients with systemic sclerosis, which is associated with decreased expression of components of the XCI machinery and increased presence of pDC subclusters with high IFN-I signature.

The authors describe the mechanism by which increased stiffness in the skin regulates the activation of pDCs, and how this process is dysregulated in patients with systemic sclerosis due to the presence of inflammatory mediators such as nucleic acid-binding chemokines.

A loss-of-function genetic screen identifies the ER-resident protein CCDC134 as an essential regulator of Toll-like receptor (TLR) responses. CCDC134 binds and stabilizes the TLR chaperone Gp96, controlling thereby the folding and trafficking of the plasma membrane and endolysosomal TLRs.

Sparano et al. show that tissue-resident NK cells produce TGF-β1 themselves to establish and maintain residency in glandular tissues. In these environments, TGF-β1, IL-15, and other factors collaboratively induce a Hobit-dependent cytotoxicity program. In the salivary glands, trNK cells limit murine cytomegalovirus persistence.

Professor Kazuyo Moro, D.D.S., PhD, finished her doctorate in the Department of Microbiology and Immunology at Keio University School of Medicine in 2007 and then worked there as a postdoctoral fellow for 5 years. She transferred to RIKEN Center for Integrative Medical Sciences (IMS) in 2012. For the first 2 years, she worked in the Laboratory for Immune Cell Systems as a senior researcher, and in 2015, she became team leader for the Laboratory for Innate Immune Systems. Since 2019, Prof. Moro holds dual appointments at RIKEN IMS and at Osaka University Graduate School of Medicine.

Sparano et al. show that tissue-resident NK cells produce TGF-β1 themselves to establish and maintain residency in glandular tissues. In these environments, TGF-β1, IL-15, and other factors collaboratively induce a Hobit-dependent cytotoxicity program. In the salivary glands, trNK cells limit murine cytomegalovirus persistence.