The present disclosure provides methods and compositions relating to isolated CD8+ T cells expressing a disease antigen-specific T cell receptor, as well as nucleic acids encoding the V? and V? polypeptide pairs of T cell receptors (TCRs) of such disease antigen-specific T cells. Such disease antigen-specific CD8+ T cells are obtainable from the periphery (e.g., blood) of a subject having a disease amenable to treatment with an IL-10 agent. The present disclosure also contemplates therapeutic methods and compositions relating to administration of isolated disease antigen-specific CD8+ T cells to a subject, as well as therapeutic methods and compositions relating to CD8+ T cells genetically modified to express a disease antigen-specific TCR and/or chimeric antigen receptor.

The present invention relates to the field of treatment of tumor, and especially to a composition comprising a plasmodium, a treatment method and an application thereof. The composition of the present invention has therapeutic effects on colorectal carcinoma, lung carcinoma, breast carcinoma, gastric carcinoma and hepatic carcinoma etc., can inhibit the growth of tumor and prolong the life of the tumor patients, whereas has no therapeutic effect on melanoma and lymphoma; meanwhile, the present invention describes that the long-term plasmodium infection has better therapeutic effect on tumors, and the plasmodium immunotherapy of the present invention does not take the fever time as a course standard when treating tumors, but should be used to extend the duration of plasmodium infection as much as possible until the progression of tumors can be controlled under the premise of protecting the organ functions and life safety of the patients.

This document provides methods and materials relating to isolated polypeptides, polypeptide preparations, vaccine preparations (e.g., anti-cancer vaccine preparations), and methods for vaccinating mammals. For example, polypeptides (e.g., CMV, MUC1, HER2, Mesothelin (MESO), TRAG-3, or CALR polypeptides) having the ability to be processed into different polypeptides such that the processed polypeptides as a group are capable of being presented by different MHC molecules present in a particular mammalian population are provided.

Contemplated immunotherapies include co-administration of an activated NK cell that is further genetically modified and a cancer therapeutic agent. In preferred embodiments, activated NK cells are further modified to taNK cells, which include a chimeric antigen receptor (CAR) with affinity for a cancer specific antigen, a cancer associated antigen, or a tumor specific antigen. Activated NK cells can also be further genetically modified to include high affinity Fc receptor CD16a (V158). Appropriate cancer therapeutic agents include chemotherapeutic drugs (e.g., nant-paclitaxel) or cancer targeted antibodies (e.g., trastuzumab).

The invention relates to methods and pharmaceutical compositions for the treatment and diagnosis of cancer. The invention also relates to methods and pharmaceutical compositions for the treatment of inflammatory diseases and autoimmune diseases. The inventors investigate the role and specific contribution of extracellular vesicles (EVs) in cancer environment. The inventors demonstrate that CSF1-associated EVs induce macrophage signature associated with T cell infiltration and extended patient survival. The inventors demonstrate that via specific extracellular vesicles, these tumors promote pro-inflammatory macrophages correlated with better clinical outcome and a better prognosis in TNBC patients. In the present invention, the inventors provide in vitro evidences towards a direct role of CSF1-associated EVs as tools, alone or with other immuno-therapies, to promote anti-tumor immune responses. Thus, the present invention relates to CSF1-associated EVs, their use in the treatment and diagnosis of cancer, and their targeting in the treatment of inflammatory diseases and autoimmune diseases.

The present disclosure relates to a novel anti-HER2 antibody or an antigen-binding fragment thereof used in the prevention or treatment of cancer, a chimeric antigen receptor including the same, and uses thereof. The antibody of the present disclosure is an antibody that specifically binds to HER2 which is highly expressed in cancer cells (particularly, breast cancer or gastric cancer cells), and binds to an epitope that is different from an epitope to which trastuzumab binds.

As disclosed herein, high expression of the inhibitory ligands Galectin-3 (LAG-3 ligand), Galectin-9 (Tim-3 ligand), HMGB1 (Tim-3 ligand), CD112 (CD112R ligand) and TNFSF10 (DR5 ligand) in the microenvironment of triple negative breast cancer cells is inhibitory for T-cells. Therefore, disclosed herein is a chimeric receptor comprising an extracellular domain of TIM-3, LAG-3, CD112R or DR5 and transmembrane and intracellular domain of a pro-inflammatory interleukin and/or a co-stimulatory domain. Also disclosed is an immune effector cell engineered to express a chimeric antigen receptor (CAR) polypeptide and the disclosed chimeric receptor. Also disclosed is a method of providing an anti-cancer immunity in a subject with a MUC1-expressing cancer, the method comprising administering to the subject an effective amount of the disclosed immune effector cell, thereby providing an anti-tumor immunity in the subject.

Disclosed herein are chimeric antigen receptors (CARs) that target MUC1*. In some embodiments, the CARs have been optimized to reduce T cell exhaustion.

Disclosed herein are chimeric antigen receptors (CARs) that target MUC1*. In some embodiments, the CARs have been optimized to reduce T cell exhaustion.

Modulators of syndecan-2, such as an antibody to syndecan-2 that cross-links syndecan-2 on the cell surface or a syndecan-2 polypeptide that interferes with syndecan-2 receptor binding, is used to regulate a Th17 mediated disease such as an autoimmune disease, fibrosis or cancer.