The present disclosure relates to a method for preparing a cancer-specific T cell based on peripheral blood or a peripheral immune organ for preventing or treating cancer, specifically including steps of: first, isolating an immune cell from peripheral blood or the peripheral immune organ; then, co-incubating with a nanoparticle and/or a microparticle loaded with a tumor whole-cell antigen for a period of time to activate the cancer-specific T cell; then, isolating a cancer-specific T cell activated by the tumor antigen; and, reinfusing the cancer-specific T cell into the body to exert an anti-cancer effect after in vitro expansion. According to the nanoparticle or microparticle prepared by the present disclosure, a tumor antigen component is loaded onto the microparticle and/or the nanoparticle to activate the cancer-specific T cell, and then the cancer-specific T cell is expanded and reinfused into a patient for treating cancer or preventing recurrence or metastasis. The cancer-specific T cell isolated by a sorting method has high specificity, and may prevent or treat cancer by killing cancer cells after expansion.

The present invention belongs to the field of biomedicine. Specifically, it provides an antibody targeting CCR8 and its applications. More particularly, the present invention offers an antibody targeting CCR8, STAR and CAR derived from the antibody, therapeutic immune cells containing the STAR or CAR, and their applications in disease treatment.

The present invention belongs to the field of biomedicine. Specifically, the present invention provides an antibody targeting Claudin18.2 and its applications. More specifically, the present invention provides an antibody targeting Claudin18.2, a STAR derived from the antibody, therapeutic immune cells containing the STAR, and their applications in the treatment of diseases.

Disclosed herein are immune effector cells for use in adoptive cell transfer that have chemically- or genetically-inhibited PDHB (Pyruvate dehydrogenase E1 subunit beta) expression or activity. Also disclosed are methods of inhibiting or ablating PDHB expression in immune effector cells ex vivo and methods of using these cells to treat subjects with cancer. In some embodiments, the immune effector cells are further treated with a TIMS inhibitor or genetically engineered to ablate TIM3 expression. In some embodiments, the immune effector cells are further treated with a LAGS inhibitor or genetically engineered to ablate LAG3 expression. In some cases, the PDHB gene is disrupted by insertion of the gene encoding the chimeric receptor into the PDHB gene loci of the cell. Therefore, disclosed herein is a chimeric cell expressing a chimeric receptor.

The present disclosure provides adoptive T cell therapies that have improved architectures for targeting antigens and recruiting multimeric immune signaling complexes for treating, preventing, or ameliorating at least one symptom of a cancer, infectious disease, autoimmune disease, inflammatory disease, and immunodeficiency, or condition associated therewith.

Recombinant NK cells, and especially recombinant NK-92 cells express a chimeric antigen receptor (CAR) having an intracellular domain of FcRI. Notably, CAR constructs with an intracellular domain of FcRI had a substantially prolonged duration of expression and significantly extended cytotoxicity over time. The CAR may be expressed from RNA and DNA, preferably as a tricistronic construct that further encodes CD16 and a cytokine to confer autocrine growth support. Advantageously, such constructs also enable high levels of transfection and expression of the recombinant proteins and provide a convenient selection marker to facilitate rapid production of recombinant NK/NK-92 cells.

Immunotherapy regimens against a viral pathogen in individuals are disclosed. The immunotherapy regimen is a universal vaccine that is administered intradermally. Multiple intradermal doses of the universal vaccine are administered to elderly individuals to prime the individual's immune system for an effective response against a viral pathogen.

A condition-controlled spliceable chimeric antigen receptor molecule and the use thereof.

The spliceable chimeric antigen receptor molecule comprises an antigen recognition unit and a signal transduction unit; the antigen recognition unit comprises an antigen recognition domain, a transmembrane domain, a costimulatory signal domain, an N-terminal splicing domain, and a degrader; and the signal transduction unit comprises a conditional signal response domain, a C-terminal splicing domain, and a signaling domain. Such a condition-controlled spliceable system can achieve splicing of the two units and signaling under a tumor microenvironment signal. The antigen recognition unit can spontaneously/be induced to degrade, thus reducing retention in normal tissues. A signaling unit can respond to a specific condition signal of a tumor microenvironment, and has the characteristics of low expression in a normal tissue environment and high expression in the tumor microenvironment. The condition-controlled spliceable system can achieve preparation of drugs and precise treatment for solid tumors by grafting different functional genes.

D domain (DD) containing polypeptides (DDpp) that specifically bind targets of interest (e.g., BCMA, CD123, CS1, HER2, AFP, and AFP p26) are provided, as are nucleic acids encoding the DDpp, vectors containing the nucleic acids and host cells containing the nucleic acids and vectors. DDpp such as DDpp fusion proteins, are also provided as are methods of making and using the DDpp. Such uses include, but are not limited to diagnostic and therapeutic applications.

Disclosed herein are polynucleotides and vectors encoding improved immunotherapeutics, polypeptides encoded by the polynucleotides and/or vectors, cells expressing the polypeptides, and pharmaceutical compositions comprising the polynucleotides, vectors, polypeptides, and/or cells.