Marta Catalfamo

TL;DR: It is demonstrated that interleukin-1 (IL-1) confers host resistance through the induction of eicosanoids that limit excessive type I interferon (IFN) production and foster bacterial containment and it is established that host-directed immunotherapy with clinically approved drugs that augment prostaglandin E2 levels in these settings prevented acute mortality of Mtb-infected mice.

TL;DR: The data support the existence of an immunoregulatory pathway wherein activated CD56(bright) NK cells inhibit T cell survival and has potential importance for the treatment of autoimmune diseases and transplant rejection and toward modification of tumor immunity.

TL;DR: It is shown that CTL and NK cells die within a few hours if they are triggered to degranulate in the presence of nontoxic thiol cathepsin protease inhibitors, which supports a model in which granule-derived surface cathePSin B provides self-protection for degranulating cytotoxic lymphocytes.

TL;DR: IL-15 acts not only as a crucial growth factor but also as an antigen-independent activator of effector functions for CD8+ memory T cells, showing that IL-15 and anti-CD3 stimulation induced remarkably similar gene expression and effector function.

TL;DR: Selfprotection of cytotoxic lymphocytes after degranulation can be explained by surface expression of the granule protease cathepsin B, as shown by suicidal degranulated cells in the presence of specific inhibitors.