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Systemic lupus erythematosus-like syndrome
Staffed by dedicated scientists with combined knowledge and expertise in antibody engineering and protein X-ray crystallography, Creative Biolabs has extensive experience in crystallizing antibody-antigen complexes and resolving their 3D structures. Based on our extensive knowledge, we are fully equipped to reach out to our clients who may have the problem or difficulty dealing with epitope mapping.

The immune system normally fights and eliminates the infectious pathogens and bacteria to keep the body healthy. An autoimmune
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Women also may experience more severe symptoms during pregnancy and with their menstrual periods. Both of these observations have led some medical professionals to believe that the female hormone estrogen may play a role in causing SLE.

Treatment for SLE
No cure for SLE exists. The goal of treatment is to ease symptoms. Treatment can vary depending on how severe your symptoms are and which parts of your body SLE affects. The treatments may include: anti-inflammatory medications for joint pain and stiffness, steroid creams for rashes,antimalarial drugs for skin and joint problems, disease modifying drugs or targeted immune system agents for more severe cases.

The reasons for the defective clearance of apoptotic cells in SLE are not clear. It could be the result of quantitative or qualitative defects of the early complement proteins, such as C2, C4, or C1q. Patients with homozygous deficiencies in these complement components develop a severe lupus-like disease early in life.129 The C1q receptors on the surface of phagocytes constitute an extremely important mechanism for the clearance of apoptotic cells.130 Patients or mice with homozygous C1q deficiency develop autoantibodies and a lupus-like syndrome apparently because of the inability to eliminate apoptotic cells effectively, which leads to an increase in the exposure of antigens to the immune system.129 131 Mice with a targeted deletion of C1q show glomerulonephritis with deposits of immune
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C1-inhibitor associated disease
Deficiency of C1-inhibitor is associated with hereditary angioedema (HAE) and acquired angioedema (AAE), Both conditions trigger recurrent angioedema which could be life threatening.

Hereditary angioedema
HAE is a disorder that leads to the recurrent attacks of severe swelling. This usually has an impact on patients’ arms, legs, face and intestinal tracts. The genetic defect is ascribed to the heterozygous deficiency of C1-inhibitor. Mutations have been identified and are reported to elicit reduced levels of C1-inhitors in the blood or lead to the production of C1-inhibitors without normal functionality.

Acquired angioedema

First described in 1972, acquired angioedema is characterized by the acquired deficiency of C1 inhibitor, hyperactivation of the classical pathway of complement system. The recurrence frequency of angioedema is not predictable. It usually lasts for two to five days and presents disfiguring, non-pruritic edema of the skin. It might affect tissues such as the face, arms genitals, buttocks, stomach, intestines or bladders

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