Contents
June 2019
Vol 4, Issue 36
Vol 4, Issue 36
Focus
- Interleukin-17 receptor D: An orphan receptor finds a home in the skin
Interleukin-17 receptor D (IL-17RD) heterodimerizes with IL-17RA to form a receptor selective for the cytokine IL-17A. (See the related Research Article by Su et al.)
- Next stop: Perivasculature! ILC2s hitch a ride on the CCL8 express
CCL8-CCR8 axis and collagen-I regulate ILC2 cells during lung inflammation. (See the related Research Article by Puttur et al.).
Research Articles
- IL-23–producing IL-10Rα–deficient gut macrophages elicit an IL-22–driven proinflammatory epithelial cell response
Proinflammatory IL-10R–deficient colonic macrophages trigger defined T cell and epithelial responses causing colitis.
- PD-1hi CD8+ resident memory T cells balance immunity and fibrotic sequelae
Exhausted-like CD8+ resident memory T cells in the lung limit immune activation–driven fibrosis.
- Pulmonary environmental cues drive group 2 innate lymphoid cell dynamics in mice and humans
Collagen-I and CCL8-CCR8 axis control the motility of ILC2s in the inflamed lung.
- Interleukin-17 receptor D constitutes an alternative receptor for interleukin-17A important in psoriasis-like skin inflammation
Interleukin-17 receptor D serves as a functional receptor for Interleukin-17A in psoriasis-like skin inflammation.
Editors' Choice
- Duel(ling) precursors in thymic Treg development
Functional thymus derived regulatory T cells can be generated by two distinct pathways.
About The Cover
ONLINE COVER Amoeboid Prowling by Lung ILC2s. Featured on the cover is a confocal image of a precision-cut mouse lung slice showing green group 2 innate lymphoid cells (ILC2s) in close proximity to peribronchial collagen fibers (in blue and magenta). Puttur et al. used intravital microscopy techniques to track the migration of ILC2s during IL-33–induced lung inflammation. These studies identify type I collagen and chemokines as key influences on the shape and locomotor activity of ILC2s during lung inflammation. [CREDIT: FRANZ PUTTUR ET AL./SCIENCE IMMUNOLOGY]