Use of an interferon (INF), whether Type I (e.g. interferon-alpha, interferon-beta, etc.), Type II (e.g. interferon-gamma) and/or Type III (e.g. interferon-lamda), for inhibiting and/or preventing coronavirus infection in people, including but not limited to those people at risk of exposure to COVID 19 and/or variants thereof.

Disclosed herein are methods of increasing response to radiation therapy in subjects afflicted with cancer. In some embodiments, the method comprises reducing the ability of an immune suppressor cell (e.g., MDSC) to migrate to the microenvironment of the cancer. In some embodiments, the method further comprises suppressing the migration of the immune suppressor cell to a non-malignant cell and/or suppressing the malignant transformation of the non-malignant cells.

Disclosed herein are methods of increasing response to radiation therapy in subjects afflicted with cancer. In some embodiments, the method comprises reducing the ability of an immune suppressor cell (e.g., MDSC) to migrate to the microenvironment of the cancer. In some embodiments, the method further comprises suppressing the migration of the immune suppressor cell to a non-malignant cell and/or suppressing the malignant transformation of the non-malignant cells.

A composition comprising TGFβ, an inflammatory agent and a tryptophan indoleamine-2,3 dioxygenase (IDO) metabolite, in particular, TGFβ, IFNγ and kynurenine, is provided, as well as regulatory mesenchymal stem cell lines or myeloid-derived suppressor cell lines obtained by contacting mesenchymal stem cell lines or myeloid-derived suppressor cell lines, respectively, with the composition. Methods for inhibiting proliferation of T cells, reducing Th17 and Tc17 differentiation of activated T cells and inflammation or for treating inter alia graft-versus-host disease (GVHD), comprising administering the cell lines, are further provided.

A composition comprising TGFβ, an inflammatory agent and a tryptophan indoleamine-2,3 dioxygenase (IDO) metabolite, in particular, TGFβ, IFNγ and kynurenine, is provided, as well as regulatory mesenchymal stem cell lines or myeloid-derived suppressor cell lines obtained by contacting mesenchymal stem cell lines or myeloid-derived suppressor cell lines, respectively, with the composition. Methods for inhibiting proliferation of T cells, reducing Th17 and Tc17 differentiation of activated T cells and inflammation or for treating inter alia graft-versus-host disease (GVHD), comprising administering the cell lines, are further provided.

One aspect of the invention provides a method of predicting whether a wound will heal. The method includes: obtaining a first measurement of a first macrophage phenotype population within a first sample obtained from a wound; obtaining a second measurement of a second macrophage phenotype population from the wound, wherein the second measurement of the second macrophage phenotype population is either: a different macrophage phenotype obtained from the first sample or the same macrophage phenotype obtained from a second, later sample from the wound; comparing the first measurement to the second measurement; and predicting whether the wound will heal based on a result of the comparing step.

The invention features methods of diagnosis by assessing B7-H1 expression in a tissue from a subject that has, or is suspected of having, cancer, methods of treatment with agents that interfere with B7-H1-receptor interaction, methods of selecting candidate subjects likely to benefit from cancer immunotherapy, and methods of inhibiting expression of B7-H1.

The present invention provides improved and/or shortened methods for expanding TILs and producing therapeutic populations of TILs, including novel methods for expanding TIL populations in a closed system that lead to improved efficacy, improved phenotype, and increased metabolic health of the TILs in a shorter time period, while allowing for reduced microbial contamination as well as decreased costs. Such TILs find use in therapeutic treatment regimens.

Provided herein are methods and compositions related to Blautia Strain A useful as therapeutic agents.

Pre-implantation factor (PIF) may be used to treat intracellular damage. Aspects of the invention are directed to a method of treating intracellular damage comprising administering PIF to a subject in need thereof. Some aspects may be directed to methods of increasing cytokine secretion in response to intracellular damage comprising administering PIF to a subject in need thereof. The intracellular damage may be a result of a disease such as Listeria monocytogenes infection, malaria, Lyme disease, cardiovascular disease, duodenal peptic ulcer, atherosclerosis, peritonitis or tuberculosis. In some aspects, a method of treating tuberculosis is disclosed, comprising administering PIF to a subject in need thereof. In some aspects, a method of treating atherosclerosis is disclosed, comprising administering PIF to a subject in need thereof. In some aspects, a method of treating peritonitis is disclosed, comprising administering PIF to a subject in need thereof.