An application of SCFV protein in preparation of a CAR gene expression vector is disclosed. The protein sequence of the SCFV protein is shown in SEQ ID No. 1. The 1st˜21st amino acids are the extracellular signal peptide amino acid sequences. The 22nd˜31st amino acids are Flag amino acid sequences. And the remaining sequences are CXCR4 scfv sequences. An application of the gene sequence encoding the SCFV protein in preparation of a CAR gene expression vector is disclosed, and the gene sequence is shown in SEQ ID No.2. A CAR gene expression vector and a CAR-T cell are disclosed. The expression vector is plent-EF1a-Flag-CXCR4 CAR, and CAR-T cells are used in the preparation of a drug for a targeted therapy of tumor cells with high expression of CXCR4.

The present disclosure relates to a composition for enhancing an immune response using the activating function of dendritic cells of a stromal vascular fraction isolated from adipose tissue, and in particular, a composition for enhancing an immune response for anti-tumor use.

Immune therapy and vaccines, such as cancer immunotherapy, or vaccines for infections with microorganisms, such as a bacterial or viral infection. In particular, the present invention relates to methods and products for prophylactic or treating cancer or infections with microorganisms by administration of specific fusion polypeptides or nucleic acids encoding such fusion polypeptides.

Chimeric antigen receptors for use in treating lymphoma-associated C-C chemokine receptor type 4 (CCR4) and other cancers expressing CCR4 are described.

Provided herein are modified NK-92 cells comprising a nucleic acid encoding C—C chemokine receptor type 7 (CCR7) operably linked to a promoter. Optionally, the cells further comprise a nucleic acid encoding C—C motif ligand 21 (CCL21), a nucleic acid encoding C—C motif ligand 19 (CCL19) or a combination thereof. Also provided are compositions and kits comprising the modified NK-92 cells. Provided are methods of making the modified cells and methods of treating cancer using the cells.

A potent human and mouse Toll-like receptor (TLR)1/TLR2 agonist was identified and optimized, Diprovocim, which exhibited an EC.sub.50 of 110 pM in human THP-1 cells and 1.3 nM in primary mouse peritoneal macrophages. In mice, Diprovocim-adjuvanted ovalbumin immunization promoted antigen-specific humoral and CTL responses, and synergized with anti-PD-L1 treatment to inhibit tumor growth, generating long-term anti-tumor memory, curing or prolonging survival of mice engrafted with the murine melanoma B16-OVA. Diprovocim induced greater frequencies of tumor infiltrating leukocytes than alum, of which CD8 T cells were necessary for the antitumor effect of immunization plus anti-PD-L1 treatment.

This invention is directed to engineered cells and methods for using the same. In embodiments, the engineered cell comprises a nucleic acid encoding a chimeric antigen receptor and a polypeptide, wherein the chimeric antigen receptor is specific for two or more antigens on the surface of a cancer cell, and wherein the polypeptide comprises an antibody or fragment thereof that can be secreted from the engineered cell.

Embodiments herein report compositions, methods, and uses for enhancing the immune system in a subject in need of such modulation/treatment. In certain embodiments, compositions and methods disclosed herein concern compositions that can include, but are not limited to, at least one agent capable of reducing the activation of, or blocking an angiotensin II receptor (ARB) and C-C chemokine receptor 2 (CCR2) and/or blocking a beta receptor (Beta Blocker, BRB), to induce and/or enhance immune response in subject. In certain embodiments, combination agents disclosed herein can enhance an immune response against cancer in a subject in need thereof. In other embodiments, combination therapies disclosed herein modify the tumor microenvironment (TME) to enhance effects of anti-cancer therapies as a combination therapy or used alone to modify the immune system of the subject to treat cancer in a subject.

This invention provides a method of reducing viral load in an HIV-1-infected human subject which comprises administering to the subject an effective HIV-1 viral load reducing dose of a CCR5 receptor antagonist, such as a humanized antibody designated PRO 140 or an anti-CCR5 receptor monoclonal antibody, wherein the viral load reducing dose achieves an average maximum decrease of viral load in the subject of at least 1.83 log.sub.10 to 2.5 log.sub.10 at about ten days following administration of the CCR5 receptor antagonist and wherein the viral load reducing dose further achieves a mean viral load reduction of 1.7 log.sub.10 at about nine days following administration of the CCR5 receptor antagonist. The viral load reducing dose results in a suppression of mean viral load by 1.0 log.sub.10 within about four days following administration of the CCR5 receptor antagonist, and suppression of viral load in the subject persists at or below a level of reduction of 1.0 log.sub.10 for about two to three weeks. This invention also provides a method of elevating CD4+ cell count in an HIV-1-infected human subject which comprises administering to the subject at a predefined interval an effective HIV-1 viral load-reducing dose of a humanized antibody designated PRO 140, or an anti-CCR5 receptor monoclonal antibody.

This invention provides a method of reducing viral load in an HIV-1-infected human subject which comprises administering to the subject an effective HIV-1 viral load reducing dose of a CCR5 receptor antagonist, such as a humanized antibody designated PRO 140 or an anti-CCR5 receptor monoclonal antibody, wherein the viral load reducing dose achieves an average maximum decrease of viral load in the subject of at least 1.83 log.sub.10 to 2.5 log.sub.10 at about ten days following administration of the CCR5 receptor antagonist and wherein the viral load reducing dose further achieves a mean viral load reduction of 1.7 log.sub.10 at about nine days following administration of the CCR5 receptor antagonist.