Lupus erythematosus (Lupus) is an autoimmune disease that involves multiple systems and organs throughout the body, with complex clinical manifestations and a recurrent disease course. The disease mostly affects women of childbearing age, and there are about one million patients in China, and the number is increasing year by year. Many lupus patients often ask the question: Is the immune system of lupus patients enhanced or reduced? Should they take immune-boosting or immune-suppressing drugs? To understand these questions, it is necessary to start with certain basic knowledge. The specific immune function in normal human includes cellular and humoral immunity, both of which are realized through immunoreactive cells. Immunologically active cells include T lymphocytes, B lymphocytes, macrophages, monocytes and natural killer cells, etc. T lymphocytes are divided into five subpopulations, each of which has its own function: in addition to cellular immunity, they mediate the balance of immunologically active cells, while B lymphocytes, under the mediation of T lymphocytes, eventually secrete antibodies in the form of plasma cells to complete humoral immunity. Macrophages and monocytes perform immune clearance functions by releasing lymphokines, secreting lysosomes and phagocytosis. Natural killer cells directly kill bacteria, viruses, intrinsic tumor cells and aberrant cells, etc., causing their lysis and death. These immunologically active cells are coordinated with each other to accomplish the immune function of the body. If any of the immune active cells and immune response links are under or over functioning, it will lead to immune abnormalities and cause a variety of immune diseases. Normal immune regulation in healthy individuals also coordinates self-tolerance and autoimmunity at a reasonable level that complements each other. When the autoimmune response is overly strong for some reason, it can also lead to damage or dysfunction of the corresponding own tissues and organs, and this pathological state is called autoimmune disease. The human immune system has the function of distinguishing between “self” and “non-self” components, and generally does not react to its own components. However, under certain special circumstances, the immune system may act on its own components and an autoimmune reaction may occur. When the autoimmune response is too strong for certain reasons, it can lead to damage or dysfunction of the corresponding own tissues and organs. If an autoimmune response causes damage to one’s own tissues and organs and a disease develops, this is often referred to as an autoimmune disease such as lupus and rheumatoid arthritis. In lupus patients, the body loses its normal immune tolerance under the influence of as yet unknown intrinsic and extrinsic factors, so that the lymphocytes cannot correctly recognize their own tissue cells and an autoimmune reaction occurs. Under normal circumstances B lymphocytes are mediated by T helper and T suppressor cells, and normal antibodies are produced. However, experiments have shown that the number of T helper and T suppressor cells in peripheral blood of lupus patients is abnormal, so that B cells are highly activated and produce a large number of autoantibodies against their own tissues (including the nucleus and various nuclear components, cell membranes, and various tissue components of the cell plasma), such as anti-nuclear antibodies, anti-Sm antibodies, anti-double-stranded DNA antibodies and anti-ribosomal antibodies, which only bind to their own tissue antigens. These autoantibodies only bind with their own tissue antigens and further form something called “immune complexes”, which circulate with the blood to the body and are activated by a substance called “complement”, causing systemic vascular inflammatory lesions, including skin vasculitis, oral ulcers, lupus nephritis, lung disease, lupus nephritis and lung disease. Autoantibodies to blood cells can cause anemia, leukocytosis or thrombocytopenia, resulting in multi-system and multi-organ functional impairment in lupus patients. Therefore, prednisone and immunosuppressants (cyclophosphamide, azathioprine and methotrexate, etc.) are emphasized in the early and middle stages of the disease to suppress the overly enhanced immune response of patients in order to bring about remission or stabilization of the disease. Immune-enhancing agents such as interferon, transfer factor and oral nuclear cheese should not be used in the early and middle stages of lupus disease. However, as lupus progresses and drugs are used, extensive vascular inflammation can cause skin and mucous membrane breakdown, easy invasion of foreign pathogenic microorganisms, and the number and activity of leukocytes, macrophages and natural killer cells are reduced, and the function of phagocytosis of bacteria is weakened. At the same time, long-term use of hormones and immunosuppressants causes reduced immune function and susceptibility to infection with foreign pathogenic bacteria. Therefore, for the middle and late stages of the disease, the immunity of patients to foreign pathogenic microorganisms is reduced, and at this time, hormones and immunosuppressive agents need to be reduced and some immune enhancers can be used appropriately. Therefore, it has been concluded that if no distinction is made between the early and middle stages of the disease, lupus is a case of enhanced immunity of “self” to “self” and “self” to “non-self”. “This is a serious and widespread immune disorder.