A method is disclosed for inducing right ventricular (RV) adaptive remodeling in a patient suffering from pulmonary hypertension (PH) due to pressure overload comprising administering a therapeutically effective amount of a carditrophin-1 polypeptide, recombinant protein or a polynucleotide encoding CT-1 polypeptide or full-length protein.

The invention relates to an anti-CD16A antigen binding protein for use in NK cell-based immunotherapy, wherein the anti-CD16A antigen binding protein is to be administered intermittently and in combination with a cytokine. In certain embodiments the antigen binding protein is a tetravalent and bispecific CD30/CD16A tandem diabody.

An implantable or injectable scaffold comprising immunostimulatory compounds and a suppressor of regulatory T cell induction is provided for use in immunotherapy treatments, including the treatment of cancers and other tumors, in particular solid tumors including inoperable tumors, as well as for other applications of immune enhancement and/or suppression.

An implantable or injectable scaffold comprising immunostimulatory compounds and a suppressor of regulatory T cell induction is provided for use in immunotherapy treatments, including the treatment of cancers and other tumors, in particular solid tumors including inoperable tumors, as well as for other applications of immune enhancement and/or suppression.

Provided are compositions and methods for production of anti-inflammatory cytokines, growth factors, or chemokines. Provided are nucleic acids (e.g., expression vectors) that include an NFκB inflammation response element operably linked to a nucleotide sequence encoding an anti-inflammatory cytokine (e.g., IL-4). In some cases, the nucleic acid is an expression vector selected from: a linear expression vector, a circular expression vector, a plasmid, and a viral expression vector. Also provided are cells (e.g., mesenchymal stem cells—MSCs) comprising a nucleic acid that includes an NFκB inflammation response element operably linked to a nucleotide sequence encoding an anti-inflammatory cytokine. In some cases, the nucleic acid is integrated into the cell's genome. Also provided are methods for treating an individual having an inflammation-associated ailment, which can include administering an MSC to the individual, where the MSC includes an NFκB inflammation response element operably linked to a nucleotide sequence encoding an anti-inflammatory cytokine.

The invention relates to methods for treating COVID-19 by targeting the inflammasome/caspase1/pyroptosis axis as a key inflammatory pathway. In particular, the invention relates to treating a patient infected with SARS-CoV-2 with an effective amount of one or more compounds that directly or indirectly inhibit one or more pathways of the inflammasome/caspase1/pyroptosis axis.

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.

Disclosed herein are methods of treatment for an intraocular pressure (IOP)-associated condition in a subject, that include administering to the subject an effective amount of a tissue plasminogen activator (tPA) therapeutic agent. In one embodiment, the IOP-associated condition is glaucoma. The administration of a tPA therapeutic agent can be an extended administration intended to cause a reduction in IOP in the subject for a period of at least one day to a year or more, relative to IOP levels in the subject prior to administration of the tPA therapeutic agent. The tPA therapeutic agent can be, for example, tPA, a tPA derivative, a small molecule direct or indirect tPA agonist, or a gene therapy vector.

This disclosure relates to compositions and methods for recruiting brown adipocytes in vitro and in vivo from brown adipocyte progenitor cells found in human skeletal muscle. Methods for treating metabolic disease are also provided. Additionally, methods for treating hypothermia are provided. In some embodiments, the brown adipocyte recruiter is a human protein or peptide. In other embodiments the brown adipocyte recruiter may be a non-human protein or peptide. In still other embodiments, the brown adipocyte recruiter is a small molecule or natural product.