The invention relates to methods of treating chronic intestinal inflammation and/or inflammatory bowel disease by administering an antagonist of oncostatin-M (OSM) and/or OSM receptor- (OSMR). The invention also relates to methods for diagnosing or prognosing chronic intestinal inflammation and/or inflammatory bowel disease in an individual and for predicting whether or not an individual will respond to an anti-TNF therapy. The methods comprise measuring OSM and/or OSMR in the individual.

Compositions and methods of activating dendritic cells with LMP1 and LMP1-activated dendritic cell based compositions and methods are effective for dendritic cell therapy and provide an adjuvant function for vaccine administration. LMP1 or LMP1-CD40 chimeric protein may be used to activate and mature dendritic cells. LMP1 and LMP1-activated dendritic cells act as an adjuvant to enhance the cellular immune response. Also disclosed herein are kits for activating dendritic cells and for preparing a vaccine formulation. Administration of the dendritic cells transfected with LMP1 can induce an immune response against cancer or infection. The mature dendritic cells may comprise an antigen and at least one cytokine in addition to LMP1. Use of LMP1 or LMP1-CD40 provides a way to activate and mature dendritic cells that retain functional and migratory abilities without the side effects that result from maturing the dendritic cells using PGE.sub.2.

Compositions and methods of activating dendritic cells with LMP1 and LMP1-activated dendritic cell based compositions and methods are effective for dendritic cell therapy and provide an adjuvant function for vaccine administration. LMP1 or LMP1-CD40 chimeric protein may be used to activate and mature dendritic cells. LMP1 and LMP1-activated dendritic cells act as an adjuvant to enhance the cellular immune response. Also disclosed herein are kits for activating dendritic cells and for preparing a vaccine formulation. Administration of the dendritic cells transfected with LMP1 can induce an immune response against cancer or infection. The mature dendritic cells may comprise an antigen and at least one cytokine in addition to LMP1. Use of LMP1 or LMP1-CD40 provides a way to activate and mature dendritic cells that retain functional and migratory abilities without the side effects that result from maturing the dendritic cells using PGE.sub.2.

The present invention relates to methods of treating disease states, including cancer, in a human comprising systemically administering a STING agonist, or a pharmaceutically acceptable salt thereof, to said human.

Aspects of the disclosure relate to methods for treating cancer, e.g., by administering to a subject having cancer a primary cell-derived biologic with multiple cytokine components in combination with an antagonist of programmed cell death-ligand 1 (PD-L1) or programmed cell death 1 (PD-1) and/or with an antagonist of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4). Other aspects of the disclosure relate to methods of identifying a subject for treatment with an antagonist of PD-L1 or PD-1 and/or an antagonist of CTLA-4 or assessing the likelihood that a subject will be responsive to an antagonist of PD-L1 or PD-1 and/or an antagonist of CTLA-4.

Aspects of the disclosure relate to methods for treating cancer, e.g., by administering to a subject having cancer a primary cell-derived biologic with multiple cytokine components in combination with an antagonist of programmed cell death-ligand 1 (PD-L1) or programmed cell death 1 (PD-1) and/or with an antagonist of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4). Other aspects of the disclosure relate to methods of identifying a subject for treatment with an antagonist of PD-L1 or PD-1 and/or an antagonist of CTLA-4 or assessing the likelihood that a subject will be responsive to an antagonist of PD-L1 or PD-1 and/or an antagonist of CTLA-4.

A method of treating cancer or metastasis is provided involving administering at least one oncostatin M (OSM) antagonist to a subject, wherein the subject has been diagnosed with cancer. Administration of an OSM antagonist such as a small molecule pharmaceutical is provided as well as an anti-OSM antibody, an anti-OSM aptamer, and an OSM mRNA antagonist. The OSM antagonists were found to inhibit or prevent tumor cell detachment, progression, proliferation and metastasis in several cancer types.

A technology regarding the production, formulation and use of conditioned media and the factors included therein is disclosed. The conditioned media may be inoculated with animal cells, plant cells and any combination thereof. The inoculations may occur simultaneous or at different times. Cells retrieved from different areas of the animal and/or the plant may also be cultured together to form conditioned media and associated growth factors.

A biological catalyst for the regeneration of tissues, obtainable directly from an adipose starting material, includes adipose material in liquid solution in a quantity of between 1.0 and 1.5 grams per millilitre of adipose starting material, in which a quantity of between 2 and 30 milligrams of proteins is present, said proteins comprising at least: from 0 to 60 picograms of PDGF, from 300 to 1300 picograms of VEGF, from 10 to 100 picograms of TGFb1, from 3000 to 7500 picograms of FGFb, from 400 to 4000 picograms of IL-1 RA. The biological catalyst is obtained from a method including at least the steps of collecting an adipose starting material; centrifuging the adipose material, to separate the collected material at least into an oily fraction, an aqueous fraction and a cellular fraction; removing the surface oily fraction; collecting the aqueous fraction and the cellular fraction, in which the above-mentioned proteins are found.

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.