The present invention belongs to the technical fields of immunology and oncologic therapies. Provided are a tumor microenvironment-regulated CAR-monocyte/macrophage, and a preparation method therefor and the use thereof. When the CAR-monocyte/macrophage forms a chimeric antigen receptor composite structure, GM-CSF can be expressed intracellularly and autocrine to extracellular to promote the differentiation of the CAR-monocyte/macrophage to form an M1 type macrophage, so that the tumor microenvironment can be further regulated while the property of resisting M2 type macrophage reversal in the tumor microenvironment is maintained, thereby sensitizing the anti-tumor effect of the CAR-monocyte/macrophage. On the basis of GM-CSF, a tumor microenvironment-regulated CAR macrophage technology platform is constructed, which can maintain the M1-type characteristics of CAR-M and can also produce a TME reversal effect, thereby achieving the efficient anti-tumor effect of a CAR-monocyte/macrophage.

The invention provides compositions and methods for treating diseases such as cancer. The invention also relates to a method of administering a therapy comprising a chimeric antigen receptor, an IL-15R molecule and an IL-15 molecule.

The invention provides compositions and methods for treating diseases such as cancer. The invention also relates to a method of administering a therapy comprising a chimeric antigen receptor, an IL-15R molecule and an IL-15 molecule.

This disclosure relates to leukocyte compositions that comprise immune cells that are modified for enhanced in vivo anti-tumor activity. The leukocyte compositions are enriched for CD4+ Th1 cells or other differentiated states and optionally depleted of CD8+ T cells.

This disclosure relates to leukocyte compositions that comprise immune cells that are modified for enhanced in vivo anti-tumor activity. The leukocyte compositions are enriched for CD4+ Th1 cells or other differentiated states and optionally depleted of CD8+ T cells.

The present disclosure provides, among other things, a method for efficiently producing natural killer cells from induced pluripotent cells. The method includes the steps of: (I) culturing pluripotent stem cells in a culture medium to produce CD56+/CD3 immune cells.

The present disclosure provides, among other things, a method for efficiently producing natural killer cells from induced pluripotent cells. The method includes the steps of: (I) culturing pluripotent stem cells in a culture medium to produce CD56+/CD3 immune cells.

The present disclosure is directed towards genetically engineered TCR-T cells to recognize tumor antigens and simultaneously secrete a binding protein that blocks an immune checkpoint molecule and TGF. These engineered T cells demonstrate stronger antitumor response and reduced T cell exhaustion. The present disclosure provides immunotherapy against HPV- or EBV-positive cancers, among others.

The present disclosure is directed towards genetically engineered TCR-T cells to recognize tumor antigens and simultaneously secrete a binding protein that blocks an immune checkpoint molecule and TGF. These engineered T cells demonstrate stronger antitumor response and reduced T cell exhaustion. The present disclosure provides immunotherapy against HPV- or EBV-positive cancers, among others.

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.