Contents
March 2019
Vol 4, Issue 33
Vol 4, Issue 33
Research Articles
- Interfacial actin protrusions mechanically enhance killing by cytotoxic T cells
Cytotoxic T cells use actin-rich protrusions at the immunological synapse to enhance perforin-mediated target cell killing.
- CD4 T cell sphingosine 1-phosphate receptor (S1PR)1 and S1PR4 and endothelial S1PR2 regulate afferent lymphatic migration
Sphingosine 1-phosphate engages multiple T cell and lymphatic endothelial cell receptors to regulate lymphocyte migration.
- Generation and persistence of human tissue-resident memory T cells in lung transplantation
Human tissue-resident memory T cells persist long term in transplanted lungs and develop from infiltrating recipient T cells.
- Tissue clonality of dendritic cell subsets and emergency DCpoiesis revealed by multicolor fate mapping of DC progenitors
Many tissue cDCs are maintained as single subset clones, which disperse upon infection with acute recruitment of pre-cDCs.
Review
- Structure and function of the immune system in the spleen
The spleen is a multitasking secondary lymphoid organ with specialized cells for initiating immunity to blood-borne targets.
Editors' Choice
- If you build it, they will come: Reaching across the “IL” with Neo-2/15
A computationally designed mimic of interleukin-2 (IL-2) selectively expands cytotoxic CD8+ T cells over regulatory T cells and supports antitumor immunity.
- T cells have seen it all before
Two recent studies demonstrate widespread preexisting immunity to Cas9 in healthy adults.
About The Cover
ONLINE COVER Clonality of the Dendritic Cell Network in Tissues. This issue's cover illustration is a Voronoi transformation of a fluorescence microscopy image showing conventional dendritic cell (cDC) clusters in the small intestine of a cDC-specific Confetti mouse. Colors depict distinct fluorescent proteins. Cabeza-Cabrerizo et al. analyze these images to show that cDCs are often organized in tissues as clusters of sister cells that must have divided locally before or after terminal differentiation. Infection can break up these clusters, in part by inducing rapid influx of cDCs precursors that intermingle into the existing mosaic. [CREDIT: MAR CABEZA-CABRERIZO AND DANIEL HEIM]