With the development of modern reproductive immunology, immune disorders have been proven to be an important cause of miscarriage, and more than 80% of patients with unexplained spontaneous abortions are related to immune factors. According to the type of immunity, recurrent miscarriages related to immune disorders can be divided into autoimmune and isoimmune types. Autoimmune recurrent miscarriages are mainly associated with autoimmune diseases such as antiphospholipid syndrome and systemic lupus erythematosus and autoantibodies. The pathogenesis of autoimmune miscarriage is mainly due to the presence of maternal autoantibodies affecting the formation and development of the fetus and placenta. The known autoantibodies associated with miscarriage are non-organ-specific antibodies and organ-specific antibodies. Non-organ-specific antibodies include antiphospholipid antibodies, anti-nuclear antibodies, anti-β2 glycoprotein antibodies, etc.; organ-specific antibodies include anti-thyroid antibodies and anti-smooth muscle antibodies, etc. Alloimmune recurrent miscarriage is associated with rejection of the embryo by the maternal immune system, including insufficient production of maternal closed antibodies, increased number of natural killer cells, and hyperfunction. It has been suggested that in normal pregnancy, the maternal-fetal interface shows immune tolerance and the gestational side is able to maintain and is associated with closed antibodies (APLA). In normal pregnancy, the paternal human leukocyte antigen (HLA antigen) carried by the embryo stimulates the mother to produce APLA. If there is an abnormality in the HLA gene and its product, resulting in the mother’s inability to recognize the paternal antigen, produce closed antibodies, and give a protective response to the embryo, it may lead to recurrent miscarriage. Further research is needed to determine whether APLA negativity should be treated. Advocates of no treatment believe that some normal pregnancies are APLA negative without adverse pregnancy outcomes such as miscarriage. Those who advocate treatment believe that APLA can bind to HLA antigens on the surface of embryonic trophoblast cells, blocking immune recognition and immune responses between mother and child, thus blocking the adverse effects of maternal lymphocytes on trophoblast cells and protecting the embryo or fetus from rejection, and that APLA can also protect and stimulate placental cell growth and differentiation, which is an important prerequisite for a successful pregnancy. How to deal with damage caused by antiphospholipid antibodies Under normal conditions, negatively charged phospholipids are located in the inner layer of the cell membrane and are therefore not recognized by the immune system. When immune disorders occur, phospholipids are exposed to the maternal immune system and various antiphospholipid antibodies are produced, including anti-cardiolipin antibodies and lupus anticoagulation factors. These antibodies bind to platelet membrane phospholipids, leading to platelet adhesion and aggregation, promoting thrombosis and subsequently inducing miscarriage. Antiphospholipid antibodies can also directly damage the vascular endothelium, leading to placental thrombosis, resulting in placental embolism and infarction. In addition, antiphospholipid antibodies act on phospholipid antigens on the surface of the trophectoderm, affecting the process of trophectoderm cell adhesion, fusion and differentiation, resulting in insufficient formation of syngeneic trophectoderm cells, leading to reduced uterine tolerance of the embryo, and subsequently leading to miscarriage. As in the aforementioned case, a patient with autoimmune recurrent miscarriage in which the presence of antiphospholipid antibodies is confirmed (the first test showed positive antiphospholipid antibodies, and the test was repeated 6 weeks later) must be promptly treated with anticoagulation. The commonly used drugs for anticoagulation in clinical practice are low-dose aspirin and low molecular heparin (LMWH). Aspirin is usually used before pregnancy at a dosage of 75-100 mg, while LMWH is recommended after pregnancy and is usually started after intrauterine pregnancy is confirmed by ultrasound, maintained throughout pregnancy and discontinued 24 hours before termination of pregnancy. There are two internationally accepted doses of LMWH: prophylactic and therapeutic. In recurrent miscarriage, the prophylactic dose of LMWH is recommended for patients without recent manifestations of vascular embolism or related medical history; the therapeutic dose is advocated for patients with recent manifestations of vascular embolism or related medical history. The prophylactic dose is up to 5000 IU of sodium heparin once/day; the therapeutic dose must be up to 200 IU/kg of sodium heparin twice/day, or up to 5000 IU of sodium heparin once/day before 16 weeks, and after 16 weeks, it is changed to 5000 IU twice/day, depending on the patient’s body weight.