Anti-Clq antibody autoantibodies

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1. The detection method used to be classical in the past: the ELISA method can bind to the auto-antibody of the CLR region of Clq, but the condition is that there must be sufficient concentration of CLR (1 ~ 10ug / ml) to ensure the binding to anti-CLR antibody, because the The difference in antigen concentration will result in different degrees of binding. For example, the binding capacity of antibodies in SLE is lower than that in HUSV.

Another detection method is to use the principle that the binding of IgG to the spherical region of Clq in 1.0M NaGl buffer will be greatly reduced, but the anti-CLR. The conjugate with Clq exists stably. The special feature of this method of using Clq solid phase analysis to detect the complex is that LOMNaCl is used during the incubation and elution of serum, which can completely remove the IgG from the immune complex to the immune complex under high salt The spherical area eluted. However, this method is far less strict and accurate than the ELISA method that uses CLR as the target antigen for detection. Therefore, the antibodies detected by this method are called Clq antibodies; and the antibodies obtained by precise methods such as ELISA are called anti-CLR antibodies. In addition, the anti-Clq antibody detected by the ELISPOT method can be used to analyze the production of antibodies at the single cell level and to study the short-term kinetic effects of anti-Clq antibodies produced by treatment.

2. Pathogenicity The pathogenicity of anti-Clq antibodies has not been known so far. The correlation between anti-CLR antibodies and lupus nephritis, especially proliferative lupus nephritis with immune deposition under the endothelium, indicates that anti-CLR antibodies are a possible causative factor. Anti-CLR antibodies are also more common in type I membranoproliferative glomerulonephritis (MPGN), which is characterized by subendothelial deposition. Anti-CLR antibodies may cause and / or continue immune deposition under the endothelial membrane by binding different Clqs located on the glomerular basement membrane; by the anti-CLR antibodies, the complexes with Clq binding will continue Increase to larger, long-standing and potentially pathogenic immune deposits.

3. The clinical significance of diseases related to anti-Clq antibodies are SLE, HUVS, rheumatoid arthritis (RA) and other rheumatic diseases and kidney diseases. The concentration of IgG anti-Clq antibody in the serum of SLE patients is 17% -46%, and the concentration of anti-Clq antibody in the serum of patients with lupus nephritis is higher than that of patients with non-lupus nephropathy. The study also found that high-titer anti-Clq antibodies are associated with the proliferation of lupus glomerulonephritis and the deposition of subendothelial immune complexes; while the concentration of anti-Clq has a weak correlation with anti-DNA or complement.

Anti-CLR antibodies are highly correlated with HUSV. In fact, patients with HUVS and SLE have IgA antibodies in their sera. Therefore, anti-CLR antibodies can be considered as a diagnostic element of HUVS.

Anti-Clq antibodies are present in the serum of only 5% of patients with simple RA, and most are IgG and low-titer IgA antibodies. Approximately 77% of patients with rheumatic vasculitis and Ferti syndrome have anti-Clq antibodies. Most of the former sera are IgA antibodies, and the latter are mostly IgG antibodies. Anti-Clq antibodies are present in the serum of other patients with rheumatic diseases such as ankylosing spondylitis, polyarteritis nodosa, and Wright's syndrome, but no anti-CLR antibodies have been found.

Approximately 73% of patients with type MPGN, 40% to 45% of type II MPGN (with electron dense deposits under the endothelium and under the epithelium) and type â…¢ MPGN (with electron dense deposits under the epithelium) have resistance CLR antibody. Anti-Clq antibodies can be found in other patients such as mesangial glomerulonephritis, focal glomerulosclerosis, and minimally diseased glomerulonephritis, but no anti-Clq antibodies have been found in IgA nephropathy patients. In fact, anti-Clq antibodies are also present in normal people, especially young people.

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