Abstract: The present disclosure relates to a method for inhibiting a STAT3 activity comprising administering SSu72 protein.

Abstract: The invention relates to a bridge assay that can be used on an automatic diagnostic apparatus in order to detect anti-thyrotropin receptor autoantibodies, wherein the chimeric TSH receptor used comprises the extracellular portion of the chimeric TSH receptor and is N-terminally fused to a protein causing secretion of the chimeric TSH receptor from culture cells, and the anchored chimeric TSH receptor is immobilized on paramagnetic particles.

Abstract: Isolated monoclonal antibodies that bind to human complement component C6 and related antibody-based compositions and molecules are disclosed. Also disclosed are therapeutic methods for using the antibodies.

Abstract: The present invention relates to the field of immunology, molecular biology and therapeutics. In particular, the invention relates to novel artificial feeder cells for activation and expansion of natural killer (NK) cells. The artificial feeder cell expresses endogenous ligands (HLA C1, C2, 5 and Bw4 type) for killer cell immunoglobulin-like receptors (KIRs), non-KIR binding Bw6 ligand, endogenous HLA-E-ligand for inhibitory NKG2A receptor, and comprises at least one stimulatory cytokine either membrane bound or secreted or at least one co-stimulatory ligand where those ligands and cytokines each specifically bind to a cognate receptor on a NK cell of interest, thereby mediating expansion of the NK cell. The invention can be used as an “off the 10 shelf” artificial feeder cell that can be readily designed to expand a NK cell or a NK subset of interest and also specifically expand NK cells modified with a chimeric antigen receptor (CAR).

Abstract: Type 1 diabetes (T1D) patients make antibodies to self-proteins that are potential biomarkers for early detection and risk prediction. We have identified seventeen antigens as biomarkers for early diagnosis and risk prediction of T1D, including the antigens MLH1, MTIF3, PPIL2, NUP50, TOX4, FIGN, C9orf142, ZNF280D, HES1, QRFPR, CTRC, SNX6, SYTL4, ELA2A, IGRP, PAX6, and HMGN3.

Abstract: Phycoerythrin (PE) and peptide:MHCII (p:MHCII) reactive monoclonal antibodies; methods to generate monoclonal antibodies including, for example, peptide:MHC (p:MHC) reactive monoclonal antibodies; compositions including monoclonal antibodies; and uses thereof.

Abstract: The present disclosure provides cells engineered to express recombinantly manufactured ultra-long acting insulin-Fc fusion proteins for use in treating diabetes. The insulin-Fc fusion proteins comprise an insulin polypeptide linked via a peptide linker to an Fc-fragment of human origin. Exemplary ultra-long acting insulin-Fc fusion proteins, cells engineered to express the fusion proteins, polynucleotides encoding these insulin-Fc fusion proteins, and pharmaceutical formulations of exemplary insulin-Fc fusion proteins are provided, in addition to methods of use and preparation.

Abstract: The present disclosure relates to a chimeric antigen receptor, a nucleic acid, a chimeric antigen receptor expression plasmid, a chimeric antigen receptor expressing cell, a pharmaceutical composition for treating cancer, and use of the chimeric antigen receptor expressing cell. The chimeric antigen receptor is specific to human leukocyte antigen G. The nucleic acid encodes the chimeric antigen receptor. The chimeric antigen receptor expression plasmid expresses the chimeric antigen receptor. The chimeric antigen receptor expressing cell is obtained by transducing the chimeric antigen receptor into an immune cell. The pharmaceutical composition for treating cancer includes the chimeric antigen receptor expressing cell and a pharmaceutically acceptable carrier.

Abstract: Disclosed are methods and compositions for determining immunodominant peptides of target enzymes used in enzyme replacement therapy for lysosomal storage disorders. More specifically disclosed are immunodominant peptides for N-acetylgalactosamine-6-sulfatase (GALNS). Also disclosed are methods of inducing oral tolerance towards a target enzyme through oral administration of immunodominant peptides prior to commencing enzyme replacement therapy. More specifically disclosed is a method of inducing oral tolerance for GALNS, by orally administering specific immunodominant peptides for GALNS; in subjects suffering from mucopolysaccharidosis type IVA prior to commencing enzyme replacement therapy using GALNS.

Abstract: Methods and reagents for diagnosing, prognosing, and treating systemic lupus erythematosus (SLE) are disclosed, involving calculating an SLE risk score for a subject based on a level of each of an erythrocyte C4d (EC4d) marker, a B-cell C4d (BC4d) marker, antinuclear antibodies (ANA), anti-Smith antibodies (anti-Sm) and optional rule-out markers (SS-B/La, Scl-70, Jo-1, CENP, MCV).

Abstract: An object of the present invention is to discover a novel peptide useful as an active ingredient in an agent for treating or preventing cancer, and to provide the use of the polypeptide as an immune inducer. The immune inducer contains as an active ingredient, the following (i) or (ii): (i) at least one polypeptide having an immune-inducing activity and selected from the group of polypeptides (a) or (b), where: (a) polypeptides consisting of 7 or more consecutive amino acids within the region of positions 24 to 97 in the amino acid sequence represented by SEQ ID NO: 2; and (b) polypeptides comprising one to several amino acid deletions, substitutions and/or additions in the amino acid sequence of any one of the polypeptides (a); and (ii) a recombinant vector comprising at least one polynucleotide encoding any one of the polypeptides, and capable of expressing the polypeptide in vivo.

Abstract: The present disclosure concerns methods and compositions related to cancer treatment comprising targeting of SRC-3 in immune cells, including T cells such as T regulatory cells. The targeting of SRC-3 in T regulatory cells in particular is effective to eradicate tumors in mammals. In specific cases, the T regulatory cells are subjected to CRISPR ex vivo to produce cells suitable for adoptive cell transfer. In some cases, one or more agents that target SRC-3 are also administered to the individual and/or are exposed to the cells prior to administration.

Abstract: Methods and materials herein are useful for assessing and/or treating autoimmune ataxias associated with septin-specific autoantibodies (e.g., septin-5-specific autoantibodies). For example, septin-5 polypeptides are provided as well as methods for using septin-5 polypeptides to detect septin-5-specific autoantibodies and/or to treat a mammal having an autoimmune ataxia.

Abstract: A pharmaceutical product containing ?2-microglobulin or a functional variant thereof as an active ingredient in the form of liposomes is provided. The product can increase the concentration of ?2-microglobulin in the blood, and can also restore a normal HC/?2-microglobulin molar ratio within membrane MHC-I complexes, or prevent a ?2-microglobulin deficit from occurring in the MHC-I complexes, of patients suffering from autoimmune diseases. Methods of treating patients with the pharmaceutical product are also presented.

Abstract: The present invention relates generally to immunotherapy. Disclosed herein are methods for obtaining cytolytic differentiated NKG2A?NKG2C+ cells with a given KIR specificity and also compositions comprising these cells as well as the use of these cells for therapy. The NK cell expansion methods provided herein also have non-therapeutic uses.

Abstract: The present invention relates to a vaccine/inhibitor combination comprising as a vaccine at least one antigen and as an inhibitor at least one inhibitor of the major histocompatibility complex (MHC) class I restricted antigen presentation. The present invention furthermore relates to a method of vaccination of a mammal using the inventive vaccine/inhibitor combination. The present invention also provides kit of parts comprising the inventive vaccine/inhibitor combination, preferably in different parts of the kit, e.g. for prior, concurrent or subsequent administration of the different parts. Additionally the invention relates to a pharmaceutical composition comprising the inventive vaccine/inhibitor combination to further improve the immune response against tumour cells and infected cells having lost the capability of MHC class I restricted antigen presentation.

Abstract: The present invention relates to CTL peptide epitopes, high-throughput methods for their identification, and their uses. In particular, the present invention relates to peptide epitopes for cancer immunotherapy and Hepatitis C Virus vaccines. The present invention also relates to methods and systems for identifying antigen-specific CTLs.

Abstract: Cord blood or peripheral blood NK cells are prepared from whole blood mononuclear cells without the need to isolate CD34+ hematopoietic stem cells or NK cells, and without the need for a feeder layer. Advantageously, the methods presented herein use an enrichment process that uses antiCD16 agonist antibodies, antiCD3 antibodies, and N-803. Moreover, contemplated processes are suitable for adaptation into a fully automated production process (GMP in a box).

Abstract: The present invention relates to the role of purinergic receptors and ATP in T cell activation and autocrine system signaling. In one embodiment, the present invention provides a method of preventing or treating diabetes by administering a therapeutically effective inhibitor of ATP to a subject. In another embodiment, the present invention provides a method of preventing or treating fibrosis by administering a P2X7R soluble fusion protein. In another embodiment, the present invention provides a method of preventing or treating graft rejection by administering an inhibitor of P2X receptor signaling.

Abstract: The present invention relates to a composition for inducing dendritic cell maturation and a method for maturing dendritic cells. More particularly, the present invention relates to a composition including a fusion protein of Rv2299c and ESAT-6, both derived from M. tuberculosis, as an active ingredient for inducing dendritic cell maturation, and a method for differentiating immature dendritic cells into dendritic cells by using the same. The method of the present invention can increase a dendritic cell immune response in the body.