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Mixed connective tissue disease caused by what?The cause of this disease is inconclusive, in of the disease associated with systemic lupus erythematosus, dermatomyositis and systemic sclerosis, mixed performance, it is independent of the disease is a disease or a disease with different subtypes, still controversial But by and large to the autoimmune theory is accepted, that may be immune dysfunction in the genetic basis of self-tissue damage, degradation and variation of the composition of autoantibodies appears to cause the immune pathological process, the reasons are: This disease and autoimmune disease systemic lupus erythematosus, dermatomyositis and systemic sclerosis have many common expression, measured by a sensitive and specific high-titer anti-RNP antibodies, epidermal basement membrane Ig at a calm, immune fluorescence examination with a similar spot with systemic lupus erythematosus-type anti-nuclear antibody, almost all positive for antinuclear antibody and other antibodies such as rheumatoid factor, antinuclear factor, also have some positive, representation in autoimmune disease kidney disease, systemic lupus erythematosus lesions, some patients can find out anti-RNP antibodies.On the pathogenesis of this disease are the following theory:
1. Genetic analysis shows that the family, all with the human leukocyte antigen-B8 (HLA-B8) who are prone to mixed collagen disease, and its suppression of T lymphocytes (T8 cells) dysfunction, some people think


may be the immune response B8 sign of control disorders, inhibition of T-lymphocytes and immune response genes, and when T lymphocyte dysfunction, immune response genes that is out of control, resulting in immune disorders (humoral and cellular immune disorders), when the suppression of T lymphocyte dysfunction, can cause hyperthyroidism humoral immunity, cellular immunity is low, T8 cells can inhibit autoimmune reactivity, its functionality once the defect, there can be self-antigen-antibody reaction, the formation of immune complexes, the formation of antigen excess soluble immune complexes, but also with the blood circulation to reach other body organs, where precipitation and cause tissue damage.
2. Viral infection viral infection result in immune dysfunction of the mechanism itself may have the following three aspects:
(1) infected T-cell cytotoxicity increased, leading to tissue destruction.
(2) virus infection in T cell function was inhibited, resulting in enhanced B cells to produce antibodies.
(3) infection of host endogenous viruses or endogenous products of HLA-B8 by the virus variant of the positive role of the host, the virus can be grown on the surface of white blood cells, resulting in anti-virus and anti-virus-infected cell responses, these response, including cellular immune response and humoral immune responses, the virus can change the composition of the emergence of their own antigen, stimulate B cells to produce the appropriate antibodies, antigen-antibody reaction occurs, the formation of immune complexes, causing tissue damage, cells infected by the virus cytotoxicity, the release of debris, the body can make its own sensitization occurs, resulting in antibodies against cellular components, while the virus can stimulate the production of lymphocytes and factors promote the occurrence of autoimmunity.
3. Anti-lymphocyte antibodies was found in mixed connective tissue disease with an anti-lymphoid serum virus antibody (anti-lymphocyte antibody), is the essence of this antibody IgM, on the surrounding T, B cells were destructive, and its activity with the surrounding Blood inverse proportion to the number of leukocytes and lymphocytes in the disease activity of its activity increased, while activity decreased in remission, with skin, nerves, positive rate of esophageal symptoms, but changes in the kidney, independent of joint symptoms.(1) skin examination shows epidermal hyperkeratosis, epithelial atrophy; dermal collagen fibers edema, hyperplasia; subcutaneous adipose tissue necrosis; subcutaneous small vessel wall thickening, intimal hyperplasia, swelling, with varying degrees of inflammatory infiltration, perivascular fibrosis, hyaline degeneration.
(2) there is degeneration of the muscle examination, striated skeletal muscle is unclear, the disease is characterized by both systemic lupus erythematosus, dermatomyositis and systemic sclerosis three comprehensive, there are differences, such as varying degrees of muscle inflammatory changes and systemic sclerosis are different; vascular inflammatory changes were a general, non-type fiber protein denaturation, is different from systemic lupus erythematosus.
5. TCM etiology and pathogenesis
(1) Etiology: the cause of this disease are no more than for the inside and outside the two-for.
More responsible for the internal deficiencies in the innate endowment, yin and yang, qi and blood deficiency or imbalance, falling dysfunction caused by organs, often triggered by the evils of the onset, or acquired partial addicted to diet, such as eat spicy Feigan born wet, heat, phlegm; or overeating cold, hurt Spleen; or Laojuan over, after the illness dystrophy; or internal injuries Chi, damage and organs, qi, etc., can lead to an imbalance of internal environment to become disease basis.
Congenital deficiency: Congenital deficiency of the people, imbalance of yin and yang, kidney yin deficiency indulge in, are the yin deficiency heat, exogenous pathogens take advantage of


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