Patent classifications
A01K2267/0325
Method of determining toxicity of an immunomodulatory drug for use in humans preliminary class
Humanized mouse models and methods are provided for determining whether administration of an immunomodulatory drug likely elicits a severe cytokine release syndrome in a human. Humanized mouse models and methods are also provided for determining the immunotoxicity in a human of a drug candidate or of drug combinations.
COMPOSITION
The present invention relates to a composition comprising a peptide derived from myelin basic protein (MBP) peptide for use in treating or preventing uveitis in a subject
HUMAN MYOSIN PEPTIDES
The present invention provides a peptide at least partially derivable from human -myosin which peptide and the use of such peptides for the prevention or suppression of autoantibody formation in myocarditis.
COMPOSITION FOR INDUCING PROLIFERATION OR ACCUMULATION OF REGULATORY T CELLS
It was found that bacteria belonging to the genus Clostridium induce accumulation of regulatory T cells (Treg cells) in the colon. Moreover, the present inventors found that regulatory T cells (Treg cells) induced by from these bacteria suppressed proliferation of effector T-cells. From these findings, the present inventors found that the use of bacteria belonging to the genus Clostridium or a physiologically active substance derived therefrom made it possible to induce proliferation or accumulation of regulatory T cells (Treg cells), and further to suppress immune functions.
COMPOSITION FOR INDUCING PROLIFERATION OR ACCUMULATION OF REGULATORY T CELLS
It was found that bacteria belonging to the genus Clostridium induce accumulation of regulatory T cells (Treg cells) in the colon. Moreover, the present inventors found that regulatory T cells (Treg cells) induced by from these bacteria suppressed proliferation of effector T-cells. From these findings, the present inventors found that the use of bacteria belonging to the genus Clostridium or a physiologically active substance derived therefrom made it possible to induce proliferation or accumulation of regulatory T cells (Treg cells), and further to suppress immune functions.
Construction Method for Immunodeficient Rat Model
A construction method for an immunodeficient rat model includes the following steps. The gRNAs targeted for knocking out a Prkdc gene and an IL2R gene are mixed with CAS9 mRNA respectively, and frozen in RNase-free ultrapure water to obtain injections A and B correspondingly. A human SIRP genomic DNA is amplified, purified, and frozen in RNase-free ultrapure water to obtain an injection C. The injections A and B are injected into cytoplasm of fertilized eggs of different rats, and the injection C is injected into a pronucleus of a fertilized egg of another rat. The three fertilized eggs are then transplanted into different pseudo-pregnant female rats to breed second-generation rats A, B and C, respectively. The second-generation rats A, B and C are intercrossed to breed an F1 generation; and the F1 generation is further intercrossed to obtain IL2R and Prkdc gene knockout immunodeficient rat models with human SIRP gene.
TRANSGENIC MICE EXPRESSING HUMAN TREM PROTEINS AND METHODS OF USE THEREOF
Provided herein are transgenic non-human animals whose genomes comprise two or more human genes selected from TREM1, TREML1, TREM2, TREML2, and TREML4, to methods of screening candidate agents that bind to and/or modulate the function and/or activity of at least one of the human genes in the transgenic non-human animals, and to methods of screening candidate agents to determine their effect on one or more activities and/or functions associated with expression of at least one of the human genes in the transgenic non-human animals. Further provided herein are methods of recapitulating a human TREM immune system in a non-human animal, and methods of generating a non-human animal disease model comprising a human TREM repertoire.
MicroRNA inhibitor therapy in systemic lupus erythematosus
Disclosed are novel compositions and methods for treating systemic lupus erythematosus (SLE) as well as a model for measuring the efficacy of said treatments. Specifically, the disclosure provides a non-human animal model for SLE comprising a severe combined immunodeficient non-human animal comprising exogenous cells from a human subject with SLE, wherein the cells from the human subject are peripheral blood mononuclear cells. Further disclosed is a method of screening for a drug candidate that inhibits or reduces SLE using a severe combined immunodeficient non-human animal.
NON-HUMAN ANIMALS HAVING A HUMANIZED B-CELL ACTIVATING FACTOR GENE
Non-human animals, cells, methods and compositions for making and using the same are provided, wherein the non-human animals and cells comprise a humanized B-cell activating factor gene. Non-human animals and cells that express a human or humanized B-cell activating factor protein from an endogenous B-cell activating factor locus are described.
HUMAN CTLA-4 ANTIBODIES AND THEIR USES
The presently subject matter provides novel human sequence antibodies against human CTLA-4 and methods of treating human diseases, infections and other conditions using these antibodies.