The present disclosure relates to genetically modified non-obese diabetic (NOD) mice deficient in murine class I MHC molecules, class II molecules, or both class I and class II MHC molecules. The MHC knockout transgenic mice provided herein are useful, for example, for developing therapies for diabetes.

Disclosed herein are nucleic acids encoding for and proteins expressing chimeric C1q polypeptides, non-human animals comprising said nucleic acids, and methods of making or using said non-human animals.

The invention relates generally to genetically modified non-human animals expressing human polypeptides and their methods of use.

Genetically modified non-human animals and methods and compositions for making and using them are provided, wherein the genetic modification comprises a deletion of the endogenous low affinity Fc?R locus, and wherein the mouse is capable of expressing a functional FcR?-chain. Genetically modified mice are described, including mice that express low affinity human Fc?R genes from the endogenous Fc?R locus, and wherein the mice comprise a functional FcR?-chain. Genetically modified mice that express up to five low affinity human Fc?R genes on accessory cells of the host immune system are provided.

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.

The present invention provides for inhibition or blockade of immunomodulatory cell receptors to facilitate improved or complete reconstitution of a human immune system in laboratory animals, improve animal health, and improve animal longevity. Thus, the invention relates generally to compositions and methods of generating and using transgenic non-human animals that are engrafted with a human hematopoietic system involving anti-CCR5 agents. In various embodiments, the human hematopoietic system engrafted transgenic non-human animals of the invention are useful as systems for the in vivo evaluation of the growth and differentiation of hematopoietic and immune cells, immune responses, vaccines and vaccination regimens, and human pathogens and production and collection of immune mediators, including human antibodies.

The instant invention is to provide a method for detecting and measuring malaria infection utilizing the induction by hemozoin (HZ); a method for screening a vaccine for malaria infection and a preventative or therapeutic agent for malaria infection using the method for detecting and measuring; and a means for regulating the induction of innate immunity using the HZ, synthetic HZ, or derivatives thereof as an adjuvant or immunostimulant. Malaria infection is detected and measured of by detecting and measuring HZ-induced, TLR9-mediated, and MyD88-dependent innate immune activity. The detection and measurement of malaria infection can be used to diagnose malaria infection. The method for detecting and measuring is also used for screening a vaccine for malaria infection and a preventative or therapeutic agent for malaria infection. Further, HZ, synthetic HZ, or derivatives thereof are used as an adjuvant or immunostimulant to regulate HZ-induced innate immune induction.

Genetically modified non-human animals comprising a human or humanized interleukin-7 (IL-7) gene. Cells, embryos, and non-human animals comprising a human or humanized IL-7 gene. Rodents that express human or humanized IL-7 protein. Genetically modified mice that comprise a human or humanized IL-7-encoding gene in their germline, wherein the human or humanized IL-7-encoding gene is under control of endogenous mouse IL-7 regulatory sequences.

Generation of chimeric non-human animals hosting bat donor cells involves chimeric mice having bat cells that may be stably tolerated to provide a new platform technology in the general field of biology, and having application in the field of immunology related to virus-host interaction, cancer biology, autoimmunity, and the development of new drugs.

The present disclosure relates to a sgRNA and constructing a dual pig model of severe immunodeficiency and liver injury and use thereof. The method comprises the steps of knocking out RAG2, IL2R? and FAH genes in a porcine fetal fibroblast by using a CRISPR/Cas9 technology, constructing a RAG2.sup.?/?/IL2R?.sup.?/Y/FAH.sup.?/? triple-gene edited cloned pig by using a somatic cell nuclear transfer technology, and obtaining a dual pig model of severe immunodeficiency and liver injury through phenotypic analysis and identification. The method overcomes the problems of long production period, low efficiency, irreversible damage, unsatisfactory use in a humanization degree and the like in the existing model construction technology, can realize a batch construction of the dual pig model of severe immunodeficiency and liver injury by a continuous cloning technology, and has great advantages and potential market application prospects in the related fields of tumor biology, cell transplantation, humanized animal models and the like.