About the Cover
Cytotoxic T cells rely on a complex system of checks and balances that modulates their activation, functional capabilities, and survival. One surface protein, SLAMF6, binds to itself in a homotypic fashion. Eisenberg and colleagues created a reagent from the ectodomain of SLAMF6 that interfered with this binding, resulting in increased activation of CD8⁺ T cells and stronger effector functions, even prolonging the survival in vivo of adoptively transferred CD8⁺ T cells, without the addition of IL2. This work provides evidence that when SLAMF6 is engaged via cell–cell contact it has an inhibitory effect on CD8⁺ T cells, which is relieved by the competitive binding of its soluble form. Read more in this issue, starting on page 127. The original confocal image is of human T cells activated with anti-CD3, with SLAMF6 (red) clustering at sites of cell–cell contact. Artwork by Lewis Long.