Contents
August 2020
Vol 5, Issue 50
Vol 5, Issue 50
Focus
- Resident TH17 cells “break bad” in kidney autoimmunity
Resident memory TH17 cells (TRM17 cells) are induced by microbial infections in kidneys and amplify renal autoimmunity.
Research Articles
- Pathogen-induced tissue-resident memory TH17 (TRM17) cells amplify autoimmune kidney disease
CD4+ TRM17 cells become activated by inflammatory cytokines to produce IL-17A and thereby promote autoimmunity.
- Functional heterogeneity of alveolar macrophage population based on expression of CXCL2
Pulmonary fungal infections generate heterogenous alveolar macrophage subpopulations.
Editors' Choice
- The (inner) world according to GARP: Genetic susceptibility and regulatory T cells
A human autoimmune and allergic disease susceptibility variant on chromosome 11 results in the reduced expression of the gene encoding the GARP protein and thus compromises the function of regulatory T cells.
About The Cover
ONLINE COVER Renal Memories of Past Infections. This month's cover is an immunofluorescence image of a thin section of mouse kidney that includes a single glomerulus consisting of a tuft of capillary endothelial cells stained for endomucin (green). The glomerular capillaries are separated from epithelial lining cells positive for synaptopodin (pink) by the glomerular basement membrane, the kidney structure that allows for filtering of the blood. Krebs et al. found that mice infected systemically with Staphylococcus aureus followed with antibiotic treatment to clear the infection maintained a stable population of kidney-resident memory T cells capable of producing IL-17A. These renal TRM17 cells could be reactivated during autoimmune kidney disease leading to exacerbated tissue damage. [CREDIT: CHRISTIAN KREBS/UKE HAMBURG]
