C1q deficiency linked to autoimmune disorders
Monday - May 2, 2011
C1q deficiency is linked to autoimmune disorders
Mouse C1q ELISA: a reliable measurement
C1q: first step in classical complement activation
- C1q is an integral part of the first component of complement (C1)
- Formation of an antibody-antigen complex (immunocomplex) activates the classical pathway of the complement system.
- C1q triggers the activation process by docking onto antibodies within these immunocomplexes
- C1q bridges the innate and adaptive immune systems
- Necrosis and apoptosis results in exposure of endogenous danger patterns, which can be directly recognized by C1q, thus activating the classical pathway
- Activated C1 cleaves complement proteins C2 and C4, resulting in the formation of C4bC2a, also called C3 convertase
C1q and diseases
- Deficiency of C1q is directly linked to Systemic Lupus Erythematosus (SLE) and glomerulonephritis due to homozygous congenital deletions
- Deficiency of C1q is associated with a higher risk of pyogenic infections
- Decrease in C1q serum levels results in reduced uptake of apoptotic cells
- The decrease of phagocytosis results in increased autoimmunity resulting in more circulating auto-antibodies
Hallmarks of mouse C1q ELISA (HK211)
- Working time of 3.5 hours
- 100 µl sample/well
- Detection limit of 15.6 ng/ml
- Useful for serum, and plasma
- Detection of unbound C1q as well as C1q-immunocomplexes (CIC)
- Cross-reactive with human and rat C1q
Linearity
The linearity of the assay was determined by serially diluting a sample containing mouse C1q. The diluted samples were measured in the assay.

Recovery
Normal mouse serum samples containing baseline levels of mouse C1q, were spiked with 50 amd 250 ng purified human C1q (Complement Technology) ranged between 101% and 102.5%.
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