Methods and compositions for treatment of malignancies are provided. The methods utilize implantation of engineered, programmable hydrogel depots capable of long-term molecule release into close proximity of the tumor. By providing gradients of immune cell chemokines and releasing immune checkpoint inhibitors, the hydrogel implants are effective at elimination of tumor cells via immune cell-mediated cell death.

An immunotherapy method of targeted chemokine and cytokine delivery by a mesenchymal stem cell that expresses an immunostimulatory factor. The immunostimulatory factor is selected from the following group: CCL3, CCL19, CCL21, XCL1, CXCL9, OX40L, 4-1BBL, GITRL, CD40L, or a combination thereof. At a tumor site, the mesenchymal stem cell specifically attracts and activates an immune cell that kills tumor tissue, and the mesenchymal stem cell has a synergistic effect with chemokines and/or cytokines, having an immunotherapeutic effect with higher efficiency and few side effects, and a significantly enhanced ability to kill tumor tissue, especially colorectal cancer cells.

The present disclosure relates to CCL22 as a T cell target in cancer immunosuppression.

The invention provides a modified CXCL9 polypeptide comprising an insertion of an additional amino acid at the N-terminus of a corresponding wild type CXCL9, a pharmaceutical composition comprising the same and a method for the production thereof and of using the same for treating cancer. Further provided nucleic acids encoding the modified CXCL9 polypeptides of the invention, vectors and host cells comprising the same.

The invention described herein relates to methods and compositions for treating cancer in a patient or a tumor cell by administering an effective amount of an anti-fugetactic agent and an additional anti-cancer agent.

The present disclosure provides immunomodulatory fusion proteins-metal hydroxide complexes comprising an immunomodulatory domain adsorbed to a metal hydroxide via ligand exchange. The disclosure also features compositions and methods of using the same, for example, to treat cancer.

The present disclosure relates to antibodies, for example monoclonal antibodies, and their use in clinical patient evaluation and therapy. The present disclosure further relates to a method for modulating the activity of human CXCL-1 protein (hereinafter, referred to as CXCL1). In an aspect, antibodies described herein are capable of being used as a medicament for the prevention and/or treatment of diseases involving CXCL1 function, for example, pathological angiogenesis and inflammatory diseases.

Contemplated treatments and methods produce substantially increased quantities of memory T-cells and a persistent immune response by subcutaneous and/or subdermal co-administration of (1) a vector comprising a recombinant nucleic acid that encodes a cancer associated epitope, a cancer specific epitope, and/or a neoepitope, (2) an immune stimulating cytokine, and (3) a checkpoint inhibitor. Most typically, the co-administration is performed at substantially the same location, preferably within 1-21 days from each other, and the vector is an adenoviral expression vector, for example, included in a viral particle such as an AdV5 virus with a deletion of the E2b gene.

The present disclosure relates to CXCR3 ligands having resistance to DPPIV and having CXCR3-expressing cell migration-inducing activity, and specifically to N-terminal amino acid modifications and N-terminal amino acid sequences that are important for resistance to DPPIV and CXCR3-expressing cell migration-inducing activity.

Featured are cells and methods of use thereof for modulating an antigen-specific immune response in a subject. The cells comprise a set of transgenes comprising two or more of PD-L1, HLA-G or H2-M3, Cd47, Cd200, FASG or FasL, Ccl21 or Ccl21b, MfgeS and Serpin B9 or Spi6, that shield the cells from immune surveillance (ie. “cloaking genes”). The cells can be used to induce immune tolerance to an antigen (e.g., a donor alloantigen or a self-antigen), or to induce an immune response to (e.g., induce the production of antibodies directed against) a non-self antigen.