A preparation method of an anti-PD-1/PD-L1 monoclonal antibody (mAb)-induced autoimmune myocarditis model is provided, including: mediating a model with adeno-associated virus 9 (AAV9) to achieve the high expression of PDL1 in a myocardial tissue, and applying an anti-PD-1/PD-L1 mAb to the model with high PDL1 expression in the myocardial tissue for modeling. The present disclosure also provides use of an animal model prepared by the preparation method. The model prepared by the present disclosure truly simulates the pathogenesis and clinical course of autoimmune myocarditis in a patient administered with an anti-PD1/PD-L1 mAb, is close to a pathophysiological status of a clinical patient, has a high modeling rate, and can be dynamically monitored.

The present invention provides transgenic animals comprising some or all components of a human heavy and/or light chain immunoglobulin variable region locus, methods of making such animals, methods of making human antibodies using such animals, and methods of treatment using the human antibodies made in such animals, wherein the animals comprise in their genome a plurality of human heavy chain V gene segments all of which are immediately preceded by the same first leader peptide-encoding sequence, and/or a plurality of human light chain V gene segments all of which are immediately preceded by the same second leader peptide-encoding sequence, or both. The invention also provides polynucleotide constructs comprising two or more human heavy or light chain leader/V gene segments comprising identical leader peptide-encoding sequences. Such animals, constructs and methods find use in efficient generation of optimally diverse populations of antibodies against antigens of interest, such as antigens of therapeutic interest.

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

Non-human animal genomes, non-human animal cells, and non-human animals comprising a humanized albumin (ALB) locus and methods of making and using such non-human animal genomes, non-human animal cells, and non-human animals are provided. Non-human animal cells or non-human animals comprising a humanized albumin locus express a human albumin protein or a chimeric albumin protein, fragments of which are from human albumin. Methods are provided for using such non-human animals comprising a humanized albumin locus to assess in vivo efficacy of human-albumin-targeting reagents such as nuclease agents designed to target human albumin.

The present disclosure relates to genetically modified non-human animals that express a human or chimeric (e.g., humanized) IL2RA, and methods of use thereof.

Non-human animals, tissues, cells, and genetic material are provided that comprise a modification of an endogenous non-human heavy chain immunoglobulin sequence and that comprise an ADAM6 activity functional in a mouse, wherein the non-human animals express a human immunoglobulin heavy chain variable domain and a cognate human immunoglobulin λ light chain variable domain.

The invention relates to a new, spontaneous mouse lymphoma cell line displaying CD19, B220, MHC II, surface IgG2a/kappa chain and MAC-1, which is negative for CD5, animal models of B-cell lymphoma based on said cell line and methods for assessing lymphoma propagation and lymphoma expansion based on said cell line.

The invention discloses a method for screening a therapeutic target of acute radiation-induced gastrointestinal syndrome and use of TIGAR target in the preparation of a medicine for treating radiation-induced gastrointestinal syndrome. The CreERT-loxP transgenic mouse model is used, in which quiescent intestinal crypt stem cells are effectively promoted to proliferate after exposure to high-dose ionizing radiation, to screen a therapeutic target that still has a therapeutic effect for radiation-induced gastrointestinal syndrome 18-24 h after ionizing radiation. Gene splicing occurs in particular cells in the CreERT-loxP transgenic mice only after the injection of tamoxifen, thereby regulating gene expression. The actual situation of initial exposure and then treatment after a nuclear accident is well simulated, so the invention is of great practical significance. The screened therapeutic target is developed into a medicine for treatment after nuclear accidents, to save precious time for the treatment after nuclear accidents.

The invention discloses a method for screening a therapeutic target of acute radiation-induced gastrointestinal syndrome and use of TIGAR target in the preparation of a medicine for treating radiation-induced gastrointestinal syndrome. The CreERT-loxP transgenic mouse model is used, in which quiescent intestinal crypt stem cells are effectively promoted to proliferate after exposure to high-dose ionizing radiation, to screen a therapeutic target that still has a therapeutic effect for radiation-induced gastrointestinal syndrome 18-24 h after ionizing radiation. Gene splicing occurs in particular cells in the CreERT-loxP transgenic mice only after the injection of tamoxifen, thereby regulating gene expression. The actual situation of initial exposure and then treatment after a nuclear accident is well simulated, so the invention is of great practical significance. The screened therapeutic target is developed into a medicine for treatment after nuclear accidents, to save precious time for the treatment after nuclear accidents.

A method for suppression of progress of, suppression of recurrence of and/or treatment of cancer, by administering an Allergin-1 antagonist in a therapy of a cancer patient with insufficient therapeutic efficacy by a tumor immunotherapeutic agent, or a cancer therapy in combination with an anti-cancer drug.