The present invention provides methods for detecting CEACAM1 expression in a cancer patient. In particular, methods according to the present invention include contacting a biological sample having Tumor Infiltrating Lymphocytes expressing CEACAM1 with an anti-CEACAM1 antibody labeled with a detectable moiety.

Provided is a method for preparing and using cell ghosts with active factors as a synergist of a lymphocyte in vitro culture. The method for preparing cell ghosts comprises: washing a cell to obtain a washed cell; and cleaving the washed cell to obtain cell ghosts, wherein the cell has cytokines capable of promoting the proliferation and differentiation of lymphocytes on their surface.

The present invention relates to a chimeric receptor capable of signaling both a primary and a co-stimulatory pathway, thus allowing activation of the co-stimulatory pathway without binding to the natural ligand. The cytoplasmic domain of the receptor contains a portion of the 4-1BB signaling domain. Embodiments of the invention relate to polynucleotides that encode the receptor, vectors and host cells encoding a chimeric receptor, particularly including T cells and natural killer (NK) cells and methods of use.

The present invention relates to an ErbB2-specific NK-92 cell or cell line containing a lentiviral vector encoding a chimeric antigen receptor and preferably two vector integration loci in its cellular genome. The present invention further relates to the use of the ErbB2-specific NK-92 cell or cell line in the prevention and/or treatment of cancer, preferably ErbB2-expressing cancers. The present invention further relates to the use of the ErbB2-specific NK-92 cell or cell line as targeted cell therapeutic agent and/or for adoptive cancer immunotherapy. The present invention further relates to a method for generating an ErbB2-specific NK-92 cell or cell line as well as to a method for identifying an ErbB2-specific NK-92 cell or cell line and to the ErbB2-specific NK-92 cell or cell line obtained or identified by the methods as well as their uses.

The present invention relates to the transient modification of cells. In particular embodiments, the cells are immune systems, such as PBMC, PBL, T (CD3+ and/or CD8+) and Natural Killer (NK) cells. The modified cells provide a population of cells that express a genetically engineered chimeric receptor which can be administered to a patient therapeutically. The present invention further relates to methods that deliver mRNA coding for the chimeric receptor to unstimulated resting PBMC, PBL, T (CD3+ and/or CD8+) and NK cells and which delivers the mRNA efficiently to the transfected cells and promotes significant target cell killing.

Provided are compositions and methods for a cell population comprising engineered cytotoxic innate lymphoid cells engineered for controlled expansion and/or activity, the engineered cytotoxic innate lymphoid cells comprising a synthetic cytokine receptor for a non-physiological ligand. The cytokine receptor may comprise a synthetic gamma chain polypeptide as a first dimerization domain, a first transmembrane domain, and an interleukin-2 receptor subunit gamma (IL-2RG) intracellular domain and a synthetic beta chain polypeptide as a second dimerization domain, a second transmembrane domain, and an intracellular domain selected from an interleukin-2 receptor subunit beta (IL-2RB) intracellular domain, an interleukin-7 receptor subunit beta (IL-7RB) intracellular domain, and/or an interleukin-21 receptor subunit beta (IL-21RB) intracellular domain. The non-physiological ligand activates the synthetic cytokine receptor in the cytotoxic innate lymphoid cells to induce expansion and/or activation of the engineered cytotoxic innate lymphoid cells.

The present invention provides a pluripotent stem cell expressing the following (a) and (b): (a) an exogenous gene encoding CC chemokine receptor 2 type B(CCR2B) (b) an exogenous gene encoding CC chemokine ligand 19 (CCL19), or an NK cell derived from the pluripotent stem cell or a progenitor cell thereof.

Described herein are multicistronic expression systems that encode chimeric proteins, specifically membrane-cleavable chimeric systems and chimeric antigen receptors. Also described herein are nucleic acids, cells, and methods directed to the same.

Disclosed herein are methods for treating solid mass tumors with direct delivery of an anti-tumor immunotherapeutic agent to the tumor site. In one aspect, this invention encompasses methods of treating solid mass tumors by direct microinjection via a microcatheter of an anti-tumor immunotherapeutic agent into the microvasculature leading into tumor thereby providing high levels of contact with the tumor while minimizing the degree of systemic buildup of the immunotherapeutic agent.

This disclosure describes, generally, a modified form of CD 16, genetically-modified cells that express the modified CD 16, and methods that involve the genetically-modified cells. The modified form of CD 16 can exhibit increased anti-tumor and/or anti- viral activity due, at least in part, to reduced susceptibility to ADAM17-mediated shedding upon NK cell stimulation.