The present invention falls within the technical field of aquaculture, and specifically, the invention relates to a specific solution for preventing and treating bacterial diseases using a Lactococcus lactis lactic acid bacterium transformed to produce an interferon type II (IFN II) immunostimulating cytokine, particularly interferon gamma (IFNg or IFNγ). Said transformed bacterium has been deposited in the Chilean Microbial Genetic Resources Collection at INIA with accession number RGM 2416 dated 22 Oct. 2017. The invention is also related to an immunostimulating food for aquaculture species comprising the lactic acid bacterium transformed with IFN type II from salmonidae. Moreover, the invention relates to the method for preparing said probiotic food, the method for preparing said lactic acid bacterium expressing IFNg, in other words which produces a cytokine that stimulates the antibacterial immune response.

The present disclosure relates to systems and methods for immune therapy. For example, a method can be used to enhance proliferation of chimeric antigen receptor (CAR) T cells in a patient, The method comprises administering to the patient an effective amount of a pharmaceutical composition comprising lymphocyte activation agents and one or more recombinant viral particles comprising a polynucleotide encoding a CAR, wherein the proliferation of CAR T cells in the patient is greater as compared to a patient administered with the one or more recombinant viral particles but without the lymphocyte activation agents.

This invention relates to methods of increasing the sensitivity of tumors to anti cancer therapies including antibody therapy, chemotherapy, radiotherapy, and therapies targeting cell signaling pathways such as the MAPK and PI3K pathways and receptor tyrosine kinases (e.g. EGFR). By increasing sensitivity of tumors to these agents, this invention will: (a)Prolong response in already responsive subjects; (b) Increase response rates by converting non-responsive patients into responsive patients; (c) Reverse treatment-induced resistance of tumors to anticancer therapy; and (d) Decrease treatment-associated toxicities by decreasing therapy dosages required for response. The invention also describes predictive tests, to identify patients most likely to respond to the combination treatments.

Compositions and methods for treating cancer are provided. In particular, the compositions comprise an anti-neoplastic agent and either an interferon type I agonist or an interferon type II agonist, or a combination of an interferon type I agonist and an interferon type II agonist.

Provided herein are methods and compositions related to the selection T cells and/or subjects for adoptive immunotherapy based on the expression of one or more biomarkers.

The present disclosure provides methods comprising administering to the individual an effective amount of an agent that decreases or inhibits TIGIT expression and/or activity and an anti-cancer agent and/or an anti-cancer therapy. Further provided are kits comprising an anti-cancer agent, an agent that decreases or inhibits TIGIT expression and/or activity, or both, as well as instructions for use thereof.

The present disclosure provides methods comprising administering to the individual an effective amount of an agent that decreases or inhibits TIGIT expression and/or activity and an anti-cancer agent and/or an anti-cancer therapy. Further provided are kits comprising an anti-cancer agent, an agent that decreases or inhibits TIGIT expression and/or activity, or both, as well as instructions for use thereof.

The present invention provides, among other things, a method of treating cancer comprising administering a GM-CSF antagonist to the patient in need of treatment, wherein the administration of the GM-CSF antagonist results in inhibition of an immunosuppressive activity of myeloid-derived suppressor cells (MDSCs). The present invention also provides, among other things, a method of inhibiting immunosuppressive activity of myeloid-derived suppressor cells (MDSCs) in a patient suffering from cancer comprising administering a GM-CSF antagonist to the patient.

Toll-like receptor (TLR) agonists can induce chemokine production. We find that TLR2 and TLR6 are widely expressed on human melanoma cells, and that TLR2/6 agonists (MALP-2 or FSL-1) synergize with interferon-gamma (IFNγ) to induce production of CXCL10 from melanoma cells. Furthermore, melanoma cells and immune cells freshly isolated from surgical specimens also respond to TLR2/6 agonists +IFNγ by upregulating CXCL10 production, compared to treatment with either agent alone. It is also disclosed herein that these compounds are useful in inducing CLXL10 in other types of cancer. Collectively, these data identify a novel synergy of TLR2/6 agonists +IFNγ for inducing CXCL10 production directly from melanoma cells, raising the possibility that intratumoral administration of these agents may improve immune signatures in melanoma and have value in combination with other immune therapies, by supporting T-cell migration into melanoma metastases.

Toll-like receptor (TLR) agonists can induce chemokine production. We find that TLR2 and TLR6 are widely expressed on human melanoma cells, and that TLR2/6 agonists (MALP-2 or FSL-1) synergize with interferon-gamma (IFNγ) to induce production of CXCL10 from melanoma cells. Furthermore, melanoma cells and immune cells freshly isolated from surgical specimens also respond to TLR2/6 agonists +IFNγ by upregulating CXCL10 production, compared to treatment with either agent alone. It is also disclosed herein that these compounds are useful in inducing CLXL10 in other types of cancer. Collectively, these data identify a novel synergy of TLR2/6 agonists +IFNγ for inducing CXCL10 production directly from melanoma cells, raising the possibility that intratumoral administration of these agents may improve immune signatures in melanoma and have value in combination with other immune therapies, by supporting T-cell migration into melanoma metastases.