The present disclosure provides, inter alia, compositions, cell populations and pharmaceutical compositions and methods useful for the treatment of inflammatory diseases or disorders. In some embodiments, the compositions, cell populations and pharmaceutical compositions and methods comprise a population of CD44.sup.+ cells modified ex vivo via treatment with a CD44 ligand for a period of time sufficient to prime the cells to produce elevated levels of one or more anti-inflammatory or immunomodulatory molecules relative to a native populations of CD44.sup.+ cells. In some embodiments, the compositions, cell populations and pharmaceutical compositions and methods comprise a population of CD44.sup.+ cells modified ex vivo via a treatment that is effective to target cells to sites of inflammation.

Provided herein are compositions containing genetically modified immune cells that express a ECM degrading enzyme, such as a matrix metallopeptidase. Overexpression of mature matrix metallopeptidase improves the tumor infiltrating capabilities of immune cells against solid tumors, including T-cells, tumor infiltrating lymphocytes, CAR macrophages, and NK cells (with and without a chimeric antigen receptor). Methods include administering CAR T or NK cells modified to express mature matrix metallopeptidase 8 to a subject with a solid tumor to improve the efficacy of the CAR T/NK cell therapy.

Provided herein are populations of placental-derived natural killer cells comprising a cleavage resistant CD16. Also provided are methods of treating diseases, disorders or conditions in a human subject comprising administering to the subject an effective amount of a population of placental-derived natural killer cells comprising a cleavage resistant CD16 to the subject so as thereby to provide an effective treatment of the to the subject. The cells, such as CYNK cells, can be placental CD34+ cell-derived natural killer (NK) cells. The diseases, disorders or conditions include cancers such as multiple myeloma and lymphoma. The present invention also provides compositions comprising populations of placental-derived natural killer cells comprising a cleavage resistant CD16 for the treatment of a subject and methods of their use.

The present disclosure provides kits and methods for tracking or monitoring in vivo biodistribution, viability, and/or expansion of immune cells in a cancer patient undergoing cellular immunotherapy.

The present disclosure provides methods and compositions that include a polynucleotide that includes nucleic acids that encode an anti-idiotype polypeptide, as well as polypeptides that are encoded by the same, and cells that include and express the polypeptide. Disclosed methods include methods that utilize the anti-idiotype polypeptides as safety switches when they are used in combination with antibodies, include approved biologic antibodies, that include the recognized idiotype. Certain embodiments include anti-idiotype polypeptides and nucleotides encoding the same, that include an internal domain. This internal domain in some embodiments has functional domains that can induce proliferation or cell death upon binding of the anti-idiotype polypeptide by its target antibody.

Provided herein are compositions and methods for reducing neuroinflammation and treating neurodegenerative diseases using proteinase inhibitors. The invention also provides methods for reducing post-injury scar formation in the central nervous system.

The present invention provides a method for treating a disease in a subject, which comprises the step of administering to the subject a plurality of cells which express: (a) a chimeric antigen receptor (CAR); and (b) a mutant version of calcineurin A and/or calcineurin B which is resistant to the calcineurin inhibitor. The subject may be receiving or have received treatment with a calcineurin inhibitor. The CAR-expressing cells may be administered prior to, following, simultaneously with or in combination with a calcineurin inhibitor.

Methods for inducing a sustained immune response against phosphorylated Tau in humans are described. The methods include administering to the subject an effective amount of liposomes including a toll-like receptor 4 agonist, a helper T-cell epitope, a lipidated CpG oligonucleotide, and a Tau phosphopeptide presented on the surface of the liposome to thereby obtain the sustained immune response.

The present disclosure describes systems and methods for immunotherapies Immune cells can be engineered to exhibit enhanced half-life as compared to control cell (e.g., a non-engineered immune cell). Immune cells can be engineered to exhibit enhanced proliferation as compared to a control cell. Immune cells can be engineered to effectively and specifically target diseased cells (e.g., cancer cells) that a control cell otherwise is insufficient or unable to target. The engineered Immune cells disclosed herein can be engineered ex vivo, in vitro, and in some cases, in vivo. The engineered Immune cells that are prepared ex vivo or in vitro can be administered to a subject in need thereof to treat a disease (e.g., myeloma or solid tumors). The engineered Immune cells can be autologous to the subject. Alternatively, the engineered immune cells can be allogeneic to the subject.

Provided are genetically engineered induced pluripotent stem cells (iPSCs) and derivative cells thereof expressing a polyethylene glycol (PEG) receptors and methods of using the same. Also provided are compositions, polypeptides, vectors, and methods of manufacturing.