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Vitlic, A.

Publications and source records attributed to Vitlic, A..

2 recordsLinked to original sources

In situ programming of intratumoural stem cell-like memory CD8+ T cells enables durable antitumour immunity in immunosuppressive tumours

Tumours with an immunosuppressive microenvironment often respond poorly to radiotherapy (RT) and immune checkpoint inhibitors, and durable clinical responses remain rare. These failures are not solely explained by insufficient immune activation, but instead reflect an inability of current therapies to establish CD8 T-cell infiltration and states required for long-term tumour control. Although stem cell-like memory CD8 T cells (Tscm) are critical for durable antitumour immunity, they are typically rare within solid tumours, and strategies to selectively augment the expansion of intratumoural Tscm within immunosuppressive tumours are lacking. Here, we show that intratumoural immune modulation via pattern recognition receptor (PRR) activation, using a double-stranded RNA-based agonist (BO-112), promotes Tscm expansion and, in combination with radiation, enhances antitumour immunity in poorly immunogenic lung and bladder cancer models. PRR activation enabled selective in situ expansion of intratumoural Tscm, rather than global CD8 T-cell activation. Therapeutic efficacy required pre-existing intratumoural CD8 T cells and was associated with qualitative reprogramming of the immune landscape, including depletion of exhausted CD8 T cells and regulatory T cells. Transcriptomic analyses showed that PRR activation preferentially enriched programmes associated with Tscm formation and self-renewal, whereas durable effector differentiation emerged only following combined RT-PRR agonist treatment, consistent with antigen-driven execution of the expanded progenitor pool. A Tscm-associated gene signature derived from these preclinical datasets correlated with improved survival across independent human lung and bladder cancer cohorts. Together, our data identify intratumoural Tscm as a therapeutically targetable immune-control axis and establish in situ programming of Tscm as a route to durable antitumour immunity.

cancer biology↗

Evidence for the Modulation of the Immune Response in Peripheral Blood Mononuclear Cells after Stimulation with a High Molecular Weight β-glucan Isolated from Lactobacillus fermentum Lf2

Lactobacillus fermentum Lf 2 produces large amounts of exopolysaccharides under optimized conditions ([~]2 g/L, EPS) which have been shown to possess immunomodulatory activity. In this study, the crude EPS was fractionated to give a high molecular weight (HMw) homoglycan and a mixture of medium molecular weight heteroglycans. The HMw EPS was isolated and identified as a {beta}-glucan.\n\nPeripheral blood mononuclear cells (PBMC) were pre-treated with purified polysaccharide to determine if the HMw {beta}-glucan is responsible for the immunomodulatory activity. Cells were also stimulated with either lipopolysaccharide (LPS) or phytohemagglutinin (PHA) and their effects, both with and without {beta}-glucan pre-treatment, compared.\n\nExposure of the cells to {beta}-glucan increased their metabolic activity and whilst a small but statistically significant drop in CD14 expression was observed at Day 1, the levels were significantly elevated at Day 2. High levels of CD14 expression were observed in cells initially exposed to the {beta}-glucan and subsequently stimulated with either LPS or PHA. In contrast, reduced levels of TLR-2 expression were observed for cells initially exposed to the {beta}-glucan and subsequently stimulated with LPS.\n\nTNF- levels were elevated in {beta}-glucan treated cells (Day1) with the levels dropping back once the {beta}-glucan had been removed (Day 2). The stimulants LPS and PHA both induced significant rises in TNF- levels, however, this induction was completely (LPS) or partially blocked (PHA) in {beta}-glucan pre-treated cells.\n\nThe results indicate a role for the bacterial {beta}-glucan in modulating the immune response following exposure to agonists such as bacterial LPS.

microbiology↗