I’m curious about how strong TCR signals (low epitope load-high affinity/high epitope load-mid affinity) relate to T cell fate. Anyone have new publications (or opinions!!) to share on that topic? #Immunosky

This is one that is unappreciated I would say. I worked in Jeroen's lab for a while. www.nature.com/articles/ni....

Control of T cell antigen reactivity via programmed TCR downregulation - Nature Immunology

Van Heijst and colleagues show that CD4+ T cells are programmed to downregulate TCR expression at the peak of clonal expansion in proportion to the strength of initial antigen recognition.

NKR and IL-15 can lower the TCR activation threshold and endow CD8+ CTLs with the ability to kill targets that express IL-15 in a non-cognate yet TCR dependent manner: www.pnas.org/doi/10.1073/...

IL-15 in tumor microenvironment causes rejection of large established tumors by T cells in a noncognate T cell receptor-dependent manner | PNAS

A major challenge of cancer immunotherapy is the persistence and outgrowth of subpopulations that lose expression of the target antigen. IL-15 is a...

I’m a big fan of this paper from the Jenkins lab. I still think of it as a relatively recent paper but now I realize it’s over 10 years old 😬 www.cell.com/cell/fulltex...

Single Naive CD4+ T Cells from a Diverse Repertoire Produce Different Effector Cell Types during Infection

Single naive T cells generate distinct ratios of macrophage and B cell helpers, based in part on the strength of signals through their unique TCRs.