Disclosed herein are methods for treating cancer comprising administering CAR-modified immune cells and at least one Retinoic Acid Receptor and/or Retinoid X Receptor active agent.

Disclosed are VIP-R antagonists for uses in managing the treatment or prevention of cancer and viral infections. In certain embodiments, this disclosure relates to chimeric variants of VIP-R antagonists, as peptides disclosed herein, and pharmaceutical composition comprising the same. In certain embodiments, this disclosure contemplates methods of treating subjects with cancer or infection with VIP-R antagonists or stimulating immune cells to target cancer by mixing immune cells in vitro with peptides disclosed herein and further administering an effective amount of stimulated immune cells to a subject in need of cancer treatment.

Provided are a novel fully human antibody for human B7H3, a chimeric antigen receptor, and uses thereof; also provided are a novel fully human anti-human B7H3 antibody, a chimeric antigen receptor containing the antibody, and genetically engineered cells expressing the receptor and the antibody. It has been verified by experiments that CAR-T, CAR-NK and CAR-iNKT cells targeting B7H3 prepared on the basis of the present chimeric antigen receptor have relatively strong proliferation ability, cytokine release ability and tumor cell killing ability, and can effectively eliminate tumor cells.

Provided is a transgenic killer cell, the genome of which is stably integrated with a coding sequence comprising an antibody of a human Fc section, or an expression cassette of a coding sequence comprising a chimeric antigen receptor or an inhibitory or agonistic antibody, and an inverted terminal repeat sequence from a transposon at both ends. Also provided is a pharmaceutical composition comprising the transgenic killer cell, and uses thereof.

Provided are antibodies to TREM2 and Gpnmb. Also provided are compositions comprising the antibodies and methods of using same.

Provided are NK-92 cells expressing a chimeric antigen receptor (CAR). The CAR can comprise an intracellular domain of Fc?RI?. Also described are methods for treating a patient having or suspected of having a disease that is treatable with NK-92 cells, such as cancer or a viral infection, comprising administering to the patient NK-92-CAR cells.

Disclosed are compositions and methods for targeted treatment of CD33-expressing cancers. In particular, chimeric antigen receptor (CAR) polypeptides are disclosed that can be used with adoptive cell transfer to target and kill CD33-expressing cancers. Also disclosed are immune effector cells, such as T cells or Natural Killer (NK) cells, that are engineered to express these CARs. Therefore, also disclosed are methods of providing an anti-tumor immunity in a subject with a CD33-expressing cancer that involves adoptive transfer of the disclosed immune effector cells engineered to express the disclosed CARs. Also disclosed are multivalent antibodies are disclosed that are able to engage T-cells to destroy CD33-expressing malignant cells.

The present invention is directed to genome editing systems, reagents and methods for immunooncology.

The presently disclosed subject matter provides methods and compositions for enhancing the immune response toward cancers and pathogens. It relates to novel designs of T cell receptors (TCRs) and engineered immunoresponsive cells comprising the same. The novel TCR binds to an antigen in an HLA-independent manner. In certain embodiments, the novel TCR provides enhanced sensitivity for a target gene having a low expression level.

Activity-inducible fusion proteins whose activity is post-translationally regulated utilizing a hsp90 binding domain and a drug molecule are described. In the absence of the drug molecule, the activity-inducible fusion proteins are inactivated but can be activated by a relevant physiological parameter in the presence of the drug molecule. Examples of the activity-inducible fusion proteins include chimeric antigen receptors (CAR) wherein the relevant physiological parameter is antigen binding.