Most patients with idiopathic thrombocytopenic purpura (idiopathic thrombocytopenic purpura, ITP) can be detected in the blood of anti-platelet antibodies, due to the lack of clear exogenous pathogenic factors, it can also be called idiopathic autoimmunity Thrombocytopenic purpura, to distinguish it from secondary autoimmune thrombocytopenic diseases. Thrombocytopenic purpura is a common clinical immune disease, mainly due to autoantibodies binding to platelets, causing increased platelet destruction. The main symptoms of ITP are bleeding in the skin and mucous membranes, decreased platelet count and shortened lifespan, normal or increased number of megakaryocytes in the bone marrow, often accompanied by developmental and maturation disorders, and antiplatelet antibodies often exist on the surface of patients' serum or platelets. According to the pathogenesis, predisposing factors, clinical manifestations, treatment effects and course of disease, ITP can be divided into acute and chronic types. The incidence of acute ITP is closely related to a variety of viral infections, while chronic ITP often occurs in women of childbearing age and is prone to relapse during pregnancy. In view of its autoimmune-related pathogenesis, the research of this disease must be based on animal models that are similar in nature to the disease.

　　Mouse Thrombocytopenic Purpura Model

　　(1) Copy method BALB/c mice weighing about 20 g and 8 weeks old. Antigen preparation: After BALB/c mice were anesthetized with ether, the eyeballs were removed and blood was taken (EDTA-Na2 anticoagulation), platelets were separated and washed, and diluted with normal saline. Immunization: Take the prepared platelets and mix the same amount of complete Freund's adjuvant and incomplete Freund's adjuvant into water-in-oil as the antigen. The antigen containing complete Freund's adjuvant was injected into the paw, back and abdomen subcutaneously of the guinea pig at week 0, at least 4 points each time, and blood was taken from the heart of the guinea pig (without anticoagulation) at week 5. Centrifuge at 560 r/min for 10 min, and take the supernatant to obtain guinea pig anti-mouse platelet serum (GP-APS), store at -20°C. Antiserum treatment: Take the APS out of the refrigerator, bath at 56°C for 30 minutes, absorb the same amount of BALB/c mouse red blood cells for at least 2 times, and dilute with normal saline to prepare different concentrations of APS. Use ELISA or agar diffusion method to detect the titer of antiserum. Antiserum (100μl) was injected into the abdominal cavity of BALB/c mice, which caused transient thrombocytopenia in mice. On the 1, 3, 5, 7, 9, 11, and 13 days after the antiserum injection, the prepared guinea pig anti-mouse platelet serum was injected into the mouse's abdominal cavity, 100 μl each time, which caused the mice to chronic and sustained thrombocytopenia. The mice were anesthetized and killed at a predetermined time, and the spleen, thymus, adrenal gland, and femur specimens were fixed with the fixative solution, and the regular tissue sections were made and observed under a microscope.

　　(2) Model characteristics After injection of antiserum, model mice may develop symptoms such as vertical hair, loose stools, weight loss, listlessness, reduced food consumption and water consumption. The model mice began to die 24 hours after modeling. The dead mice showed bleeding in the abdominal cavity, intestines, and urethra, and massive bleeding points in the posterior peritoneum; 1 to 3 days after modeling was the peak death time of mice. Animal death and various bleeding manifestations are more common within 7 days after injection of antiserum. After antiplatelet serum is injected into model mice, it can cause a significant decrease in platelet count. Platelet-associated antibody (PAIgG) is elevated. The weight of the spleen of mice began to increase at 6h after injection, and the weight of the spleen was 3.6 times that of normal mice on the 5th day. The megakaryocytes of the spleen began to increase significantly on the 6th day after the antiserum injection, and remained at a high level on the 15th day, and then tended to normal; the increase in spleen weight was significantly consistent with the increase in megakaryocytes. Microscopic histopathological observations showed that megakaryocytes were seen in the bone marrow tissue at 6 hours after modeling, reaching a peak on the 3rd day, and still higher than normal mice at 22 days. A quarter of the model mice showed atrophy of thymus and adrenal cortex. After the model was established, the mice developed obvious subcutaneous purpura, focusing on the injection site (abdomen), scrotum, limbs, and tail. The mouse (or rabbit) thrombocytopenic purpura model established by this method (immune method) has simple production principles, more complicated operating methods, small interference factors, and relatively low cost. However, the antibodies are exogenous and need to be continuously supplemented and infused, and the stability of chronic ITP is relatively poor. The effect is better than previous thrombocytopenia animal models replicated by ADP, Marilan, cyclophosphamide or radiation irradiation. Although the models established with ADP, Marilan, cyclophosphamide and other methods can also cause thrombocytopenia, these replication methods are by damaging the bone marrow hematopoietic stem cells of model animals, resulting in the reduction of bone marrow and peripheral blood triline cells to replicate thrombocytopenia The pathogenesis and clinical manifestations of the model are not exactly the same as those of ITP. In the study of the efficacy or pharmacology of new drugs for the treatment of ITP, it can directly affect the judgment of the efficacy. The key to the application of this method to replicate ITP animal models lies in the purification of platelet antigens. The immune pathways and methods can directly affect the titer of APS.

　　(3) Comparative medicine Primary thrombocytopenic purpura is a common clinical bleeding disease, characterized by peripheral thrombocytopenia, bone marrow megakaryocyte proliferation and maturation disorder. Since antiplatelet antibodies can be detected in the blood of clinical patients, it is also called immune thrombocytopenic purpura. The pathogenesis is due to the binding of the same antibody or autoantibody to the platelet membrane antigen, which causes increased platelet destruction and disease. Therefore, the detection of platelet antibodies is very important in the diagnosis and efficacy determination of ITP disease. The clinical treatment of this disease is mainly the use of corticosteroids, immunosuppressants and splenectomy. From the perspective of long-term efficacy, most patients still cannot obtain complete ease. Therefore, breakthroughs in basic and clinical research are urgently needed. At present, the clinical research mainly focuses on PAIgG. The animal model of chronic ITP established by injection of exogenous antibodies shows similar characteristics to patients with clinical human ITP. When the antiplatelet serum is injected into the model animal, it causes a significant decrease in the platelet count and an increase in the level of PAIgG; the more antiserum injected, the greater the increase in PAIgG and the more severe the thrombocytopenia. At the same time, the lifespan of platelets of model animals is shortened, accompanied by fever, purpura and hemostatic disorders. This model has great application value for the research of human ITP pathogenesis and the screening of anti-thrombocytopenia drugs.