Provided is a method for preparing genetically-modified T cells expressing chimeric antigen receptor, comprising: (i) a step of preparing non-proliferative cells holding a viral peptide antigen, which are obtained by stimulating a group of cells comprising T cells using an anti-CD3 antibody and an anti-CD28 antibody followed by culturing in the presence of the viral peptide antigen and a treatment for causing the cells to lose their proliferation capability; (ii) a step of obtaining genetically-modified T cells into which a target antigen-specific chimeric antigen receptor gene has been introduced using a transposon method; (iii) a step of mixing the non-proliferative cells prepared by step (i) with the genetically-modified T cells obtained by step (ii), and co-culturing the mixed cells; and (iv) a step of collecting the cells after culture.

The present invention provides a medicine containing a Toll-like receptor agonist, LAG-3 protein, a variant or derivative thereof.

The present invention provides a medicine containing a Toll-like receptor agonist, LAG-3 protein, a variant or derivative thereof.

The invention relates to the formulation of pharmaceutical compositions of etanercept. The invention also relates to methods of removing buffer and of formulating pharmaceutical compositions of etanercept.

Based on the identification of IL-33 as an exacerbating factor in endometriosis and adenomyosis uteri, a therapeutic agent for endometriosis and adenomyosis uteri has an IL-33 antagonist, which is capable of inhibiting the function of IL-33. The IL-33 antagonist is useful for treating, preventing or alleviating endometriosis and uterine adenomyosis uteri.

Provided herein are improved gene therapy vectors and methods of use, in some embodiments, comprising sequences for improved expression and cellular targeting of a therapeutic protein.

Provided herein are improved gene therapy vectors and methods of use, in some embodiments, comprising sequences for improved expression and cellular targeting of a therapeutic protein.

The invention provides a method for treating cancer comprising the step of administering a therapeutically effective amount of KPC1, a peptide which is at least about 70% homologous to the KPC1 or an agent which up-regulates KPC1. In some embodiments, there is also provided a method for treating cancer comprising the step of administering a therapeutically effective amount of p50, a peptide which is at least about 70% homologous to the p50 or an agent which up-regulates p50.

The invention provides a method for treating cancer comprising the step of administering a therapeutically effective amount of KPC1, a peptide which is at least about 70% homologous to the KPC1 or an agent which up-regulates KPC1. In some embodiments, there is also provided a method for treating cancer comprising the step of administering a therapeutically effective amount of p50, a peptide which is at least about 70% homologous to the p50 or an agent which up-regulates p50.

Described herein are compounds and methods for tethering proteins. For example, dimers of Protein X listed in Table 1 are described, where the dimers are formed by the covalent bonding of a cysteine on the first monomer to a cysteine on the second monomer via a cyclic disulfide linker. The covalently attached dimers exhibit increased stabilization and can be used to treat neurodegenerative diseases (such as, for example, Parkinson's Disease, ALS, Alzheimer's Disease, Huntington's Disease, Epilepsy, Frontotemporal Dementia, and/or DMD), cancer, autoimmune disease, and/or Celiac disease.