The present disclosure relates to promoter constructs comprising: one or more heat shock elements: a core promoter; and a gene of interest: vectors comprising the promoter constructs, and immune cells modified to include the promoter constructs. The promoter constructs provide the ability to remotely control immune cell therapies by thermal targeting. The present disclosure also provides methods of use for the promoter constructs.

The present disclosure relates to the technical field of medicines, and particularly relates to an immune preparation, a composition comprising the immune preparation and a use thereof, and a preparation method. an immune adjuvant provided by the present disclosure is an erythrocyte-derived vesicle, and the erythrocyte-derived vesicle has an erythrocyte content and a biofilm structured wrapped outside the erythrocyte content as a whole, and the two are matched with each other, so that the erythrocyte-derived vesicle serves as an endogenous substance of the body to activate an immune system of the body and effectively enhance a cellular immune response. Moreover, in this process, no toxic or side effect is caused to the body, and the method has the advantages of high biocompatibility, safe raw material source and simple preparation process.

Provided are methods and compositions for obtaining functionally enhanced derivative effector cells obtained from directed differentiation of genomically engineered iPSCs. Embodiments of derivative cells provided herein have stable and functional genome editing that delivers improved or enhanced therapeutic effects. Also provided are therapeutic compositions and the use thereof comprising functionally enhanced derivative effector cells alone, or with antibodies or checkpoint inhibitors in combination therapies.

This disclosure describes a novel kick and kill strategy as an effective cancer therapy for treating virus-associated cancers. In particular, this disclosure provides a method of reactivating a latent Epstein-Barr virus (EBV) in a cell infected with the EBV. Also provided are a method of eliciting or enhancing an immune response against an EBV-positive cancer cell in a subject infected with the EBV and a method of treating a subject having cancer associated with EBV infection.

The present invention provides methods for expanding TILs and producing therapeutic populations of TILs. According to exemplary embodiments, at least a portion of the therapeutic population of TILs are gene-edited to enhance their therapeutic effect. According to further embodiments, methods for gene-editing TILs include intratumoral delivery of expression vectors for immune checkpoint inhibitors using an electroporation system prior to harvesting the tumor for TIL production. According to yet further embodiments, an adjuvant therapy for cancer includes delivery of expression vectors for immune checkpoint inhibitors before, after or before and after infusion of TILs for treating cancer.

The present invention provides improved and/or shortened processes and methods for preparing TILs in order to prepare therapeutic populations of TILs with increased therapeutic efficacy for the treatment of cancer with TILs in combination with CT-LA-4 and PD-1 inhibitors and/or PD-L1 inhibitors as described herein.

Disclosed herein is a method for predicting the responsiveness of a subject to CD40 agonist therapy, such as agonist anti-CD40 therapy, that involves assaying a tumor sample from the subject for a 12 Chemokine gene signature demonstrating that the tumor comprises tertiary lymphoid structures containing B cells. Therefore, also disclosed herein is a method of treating tumors, such as solid tumors, in a subject that involves administering to the subject an effective amount of a composition comprising assaying a tumor sample from the subject for a 12 Chemokine gene signature demonstrating that the tumor comprises tertiary lymphoid structures (TLS) containing B cells, and treating the subject with CD40 agonist therapy, such an agonist anti-CD40 antibody.

The present invention relates to a Leukocyte-specific protein 1 (LSP1)-deficient T cell-based anticancer immunotherapy. According to the present invention, tumor growth, tumor volume and size were reduced by means of LSP1 knockout, and LSP1 deficiency in T cells increases the number, distribution frequency, migration, and invasion of T cells, and increases the production of an anti-tumor cytokine to inhibit tumor growth and enhance tumor-killing ability. Thus, the present invention can be used for T cell-based immunotherapy.

The present invention relates to the treatment or management of autoimmune disorders, organ rejection and cancers utilizing CAR constructs that bind to T-cell surface antigens or B-cell or plasma surface antigens or both.

Compounds, compositions and methods are provided for the inhibition of ENPP1. Aspects of the subject methods include contacting a sample with a cell impermeable ENPP1 inhibitor to inhibit cGAMP hydrolysis activity of ENPP1. Aspects of the methods include administering to a subject in need thereof a therapeutically effective amount of a CAR expressing immune cell in combination with a therapeutically effective amount of a cell impermeable ENPP1 inhibitor to inhibit the hydrolysis of cGAMP.