Activated T cells release bioactive Fas ligand (FasL) in exosomes, which subsequently induce self-apoptosis of T cells. However, their potential effects on cell apoptosis in tumors are still unknown. In this study, we purified exosomes expressing FasL from activated CD8+ T cell from OT-I mice and found that activated T cell exosomes had little effect on apoptosis and proliferation of tumor cells but promoted the invasion of B16 and 3LL cancer cells in vitro via the Fas/FasL pathway. Activated T cell exosomes increased the amount of cellular FLICE inhibitory proteins and subsequently activated the ERK and NF-κB pathways, which subsequently increased MMP9 expression in the B16 murine melanoma cells. In a tumor-invasive model in vivo, we observed that the activated T cell exosomes promoted the migration of B16 tumor cells to lung. Interestingly, pretreatment with FasL mAb significantly reduced the migration of B16 tumor cells to lung. Furthermore, CD8 and FasL double-positive exosomes from tumor mice, but not normal mice, also increased the expression of MMP9 and promoted the invasive ability of B16 murine melanoma and 3LL lung cancer cells. In conclusion, our results indicate that activated T cell exosomes promote melanoma and lung cancer cell metastasis by increasing the expression of MMP9 via Fas signaling, revealing a new mechanism of tumor immune escape.

The effects of a sodium (Na) promoter on the catalytic performance of cobalt-manganese (CoMn) catalysts for Fischer–Tropsch to olefin (FTO) reactions were investigated. For the sample without Na, Co0 was found to be the active phase for the traditional Co-based Fischer–Tropsch reaction with low CO2 selectivity. The olefin/paraffin (O/P) ratio was found to be low with a C2–4 = selectivity of only 15.4 C%. However, with the addition of Na, cobalt carbide (Co2C) quadrangular nanoprisms with the (101) and (020) facets exposed were formed. The Co2C nanoprisms displayed a high C2–4 = selectivity (54.2 C%) as well as a low methane selectivity (5.9 C%) under mild reaction conditions. The O/P ratio for C2–4 reached 23.9, and the product distribution deviated greatly from the classical Anderson–Schulz–Flory (ASF) distribution. Co2C nanoprisms were considered to be an effective FTO active phase with strong facet effects. The Na promoter played a key role in the evolution of the FTO catalysts. The addition of Na, which acted as an electronic donor to cobalt, resulted in stronger CO adsorption and enhanced CO dissociation, which also benefited the formation of the Co2C phase, leading to highly stable and active catalysts. The effects of other alkali promoters were also studied, and only the K promoter had an effect similar to that of Na on the CoMn catalysts for promoting the FTO reaction.

How the intestinal tract develops a tolerance to foreign antigens is still largely unknown. Here we report that extracellular vesicles (EVs) with TGF-β1-dependent immunosuppressive activity are produced by intestinal epithelial cells (IECs) under physiological conditions. Transfer of these EVs into inflammatory bowel disease (IBD) mice induced by dextran sulfate sodium salt decreases IBD severity by inducing regulatory T cells and immunosuppressive dendritic cells. In contrast, decreased endogenous EV production promotes IBD development. IECs produce EVs with increased levels of TGF-β1 upon IBD development in an ERK-dependent manner. Furthermore, these EVs tend to localize in the intestinal tract associated with epithelial cell adhesion molecule (EpCAM). Knockdown of EpCAM in vivo increases the severity of murine IBD, and the protective effect of EVs from IECs with decreased EpCAM on murine IBD is blunted. Therefore, our study indicates that EVs from IECs participate in maintaining the intestinal tract immune balance.