Contents
May 2019
Vol 4, Issue 35
Vol 4, Issue 35
Focus
- Igniting the flame in arthritis: C5aR2 controls endothelial transcytosis of C5a
C5aR2 transfers arthritic joint-derived C5a to the blood vessel endothelium to start C5aR1-driven neutrophilic inflammation. See related Research Article by Miyabe et al.
Research Articles
- Atypical complement receptor C5aR2 transports C5a to initiate neutrophil adhesion and inflammation
C5aR2 transports C5a into the blood vessel lumen to initiate neutrophil arrest in a murine model of arthritis.
- Human natural killer cells mediate adaptive immunity to viral antigens
Vaccination or childhood infection elicits antigen-specific, long-lived immunological memory in human natural killer cells.
- Distinct immunocyte-promoting and adipocyte-generating stromal components coordinate adipose tissue immune and metabolic tenors
Adipose tissue Tregs dynamically dialogue with stromal cells via the ST2:IL-33 axis in homeostasis and disease.
- Stromal cells maintain immune cell homeostasis in adipose tissue via production of interleukin-33
Tissue-resident stromal cells control innate lymphoid cell–dependent immune homeostasis in adipose tissue.
Editors' Choice
- Y’all comeback now
Keratinocytes regulate circulating CD8+ T cell memory after cutaneous infection.
- Is your immune system over the hill?
Longitudinal study of immune function yields cytometric and transcriptomic measures of immune age.
About The Cover
ONLINE COVER Adiposphere Mound. This month's cover shows a stack of two 3D organoids grown from distinct subtypes of mesenchymal stromal cells found in visceral adipose tissue. These spherical organoids were generated using adipogenic media and stained with dyes that bound to nuclear DNA (blue) or fat droplets (green). Spallanzani et al. used single-cell RNA sequencing to identify which subtypes of stromal cells within white fat make interleukin-33 (IL-33), a cytokine that supports maintenance of regulatory T cells and group 2 innate lymphoid cells within visceral adipose tissue. [CREDIT: RAUL GERMÁN SPALLANZANI]
