The present invention provides compositions and methods for selective inhibition of the classical or non-classical LTβR-NFκB signaling pathway. In some embodiments, the compositions and methods of the present invention are useful for treating or preventing tissue graft rejection, inflammation, contact hypersensitivity, and cancer by decreasing cell motility.

The present invention provides nucleic acids, vectors, host cells, methods and compositions to confer and/or augment immune responses mediated by cellular immunotherapy, such as by adoptively transferring CD8+ central memory T cells or combinations of central memory T cells with CD4+ T cells that are genetically modified to express a chimeric receptor. In some alternatives the genetically modified host cell comprises a nucleic acid comprising a polynucleotide coding for a ligand binding domain, a poly nucleotide comprising a customized spacer region, a polynucleotide comprising a transmembrane domain, and a polynucleotide comprising an intracellular signaling domain. In some alternatives, the ligand binding domains binds to CD171.

Methods of treating an ischemic disease in a subject are provided. Accordingly there is provided a method comprising administering to the subject a therapeutically effective amount of cells with reduced level of expression and/or activity of TNFR1, thereby treating the ischemic disease in the subject. Also provided is a method comprising treating with TNFalpha cells with reduced expression and/or activity of TNFR1 and administering to the subject a therapeutically effective amount of said cells, thereby treating the ischemic disease in the subject.

The present invention relates to an antibody specific for CD22 and uses thereof, and more particularly to an antibody that specifically binds to CD22, a chimeric antigen receptor comprising the antibody, a CAR-T cell expressing the chimeric antigen receptor, and a pharmaceutical composition for preventing or treating diseases mediated by cells expressing CD22 including the same.

It was confirmed that the antibody selected in the present invention specifically recognized CD22-expressing cells, and the chimeric antigen receptor (CAR) and CAR-T cells targeting CD22 using the CD22-specific antibody not only effectively bound to CD22, but also activated CAR-T cells bound to CD22. In addition, since it was confirmed that the CAR-T cells of the present invention effectively kill CD22-expressing cells, the CD22-specific antibody, the chimeric antigen receptor targeting CD22, and CAR-T cells of the present invention can be usefully used as a composition for preventing or treating diseases relating to CD22 expression.

As a technique enabling to simply and accurately diagnose human T cell leukemia virus type 1 (HTLV-1) related disease, there is provided a diagnostic method for an HTLV-1 related disease based on an amount of tumor necrosis factor receptor 2 (TNFR2) in a blood sample taken from a subject, wherein (1) it is determined based on an increase of the amount of TNFR2 that the subject suffers from, or is likely to develop, the HTLV-1 related disease; and/or (2) it is determined based on a decrease of the amount of TNFR2 that the subject is in remission, or is likely to be in remission, of the HTLV-1 related disease.

The present disclosure provides T-cell modulatory multimeric polypeptides comprising two different immunomodulatory polypeptides, at least one of which is a variant immunomodulatory polypeptide. The present disclosure provides nucleic acids comprising nucleotide sequences encoding the T-cell modulatory multimeric polypeptides, and host cells comprising the nucleic acids. The present disclosure provides methods of modulating the activity of a T cell; the methods comprise contacting the T cell with a T-cell modulatory multimeric polypeptide of the present disclosure.

Provided is a chimeric antigen receptor targeting CLL1 and an application thereof. The chimeric antigen receptor targeting CLL1 comprises an antigen binding domain, a hinge region, a transmembrane domain and a signal transduction domain; the antigen binding domain is an anti-CLL1 antibody. The present application uses an anti-CLL1 antibody as the antigen binding domain to construct a chimeric antigen receptor molecule, the chimeric antigen receptor targeting CLL1 has specific targeting effect on CLL1 positive tumor cells, and immune cells expressing chimeric antigen receptor targeting CLL1 have a significant killing effect in vitro and in vivo, and secrete a large amount of cytokine IFN-γ after co-cultured with CLL1 positive tumor cells, which has a specific clearance effect on CLL1 positive tumor cells.

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.

The present invention relates to polymeric nanoparticles comprising a cytokine or a nucleic acid encoding for a cytokine, pharmaceutical compositions comprising the same, and methods for treating certain diseases comprising administering these polymeric nanoparticles to a subject in need thereof.

The present disclosure relates to genetically modified non-human animals that express a human or chimeric (e.g., humanized) TNFR2, and methods of use thereof.