This disease is the body's endogenous (self) antigen by the immune complex
diseases and disorders associated with T cell function. To be investigated in
the patients serum antibodies have a variety of anti-autologous tissue
composition, including anti-DNA antibodies, especially anti-double stranded DNA
(natural DNA) antibody is more effective than positive, patients with
circulating immune complexes separable into natural and single-stranded DNA
antibodies and antigens; eluted from glomerular immunoglobulin antibody can be
combined with natural and single-stranded DNA antigen.
A humoral immune changes in which DNA and anti-DNA antibodies form immune
complexes play a major role. (1) virus triggering factors: more studies confirm
the disease is an RNA virus - type C virus. C-type virus on the one hand may
damage the cells, so that the release of DNA was highly immunogenic; the other
hand, may be due to this virus reverse transcriptase, the virus's own RNA copied
into DNA, leaving the body to produce anti-DNA antibodies, both anti-viral
replication generated by DNA, but also against human DNA. (2) Bacterial toxins
and lipopolysaccharide trigger factors: Some bacterial lipopolysaccharide
composition injected into mice and observed that can contribute to the DNA of
mouse tissue release to the blood circulation and the role of mitogen to promote
the activation of B lymphocytes to produce antibodies, so that these substances
promote the role of DNA antigen-antibody complex to generate. (3) autologous
tissue damage to the release of DNA: the patients in vivo lymphocyte cytotoxic
antibodies. Medium molecular weight soluble DNA immune complexes through the
blood circulation to the kidneys (or other organs) and deposited in the
glomerulus.
Cellular immunity: the suppressor T cell function and decline in the number.
The reason is that the existence of cytotoxic antibody (anti-lymphocyte or
thymocyte antibody) in serum, thereby undermining the T cells. Decreased
suppressor T cells, on the one hand, to reduce the inhibition of antibody
formation, on the other hand may be due to the release of lymphokines decreased
to inactivate the ability of helper T cells, helper T cells to promote antibody
production capacity increase, the total The humoral immune (antibody formation)
strong.
(3) genetic factors, patients who have family history of the same disease
accounted for 0.4% to 3.4.
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