Comprehensive Complement System Component Testing Service
The complement system is a sophisticated cascade reaction system composed of nearly 40 proteins, serving as a core component of the body's innate immunity. It functions like a "precision-guided missile system" within the immune defense network. Activated via the classical, alternative, and lectin pathways, it ultimately forms the Membrane Attack Complex (MAC) to directly lyse pathogens or abnormal cells, while also performing critical functions such as opsonization, mediation of inflammation, and clearance of immune complexes.
The concentration and functional activity of complement components are vital indicators for assessing innate immune function and diagnosing related disorders. Abnormal levels (often manifesting as decreases in key components like C3 and C4) are commonly observed in various autoimmune diseases, acute/chronic infections, kidney diseases, and hereditary complement deficiencies. Our complement component detection service aims to provide crucial immunological evidence for your clinical diagnosis and mechanistic research through precise quantitative analysis.
Our Services
Creative Diagnostics offers comprehensive quantitative testing of complement components. The table below outlines the main detection items, their roles within the complement activation pathways, and their clinical significance.
| Detection Item | Primary Function & Pathway Role | Clinical Significance |
| C1q | The initiator of the classical pathway; recognizes antibody complexes. | Decreased: Seen in active Systemic Lupus Erythematosus (SLE), hereditary C1q deficiency, certain vasculitides. A key correlate in lupus nephritis. |
| C3 | The central hub of the complement system; all three activation pathways converge here, leading to its cleavage. | Decreased: Most common in active SLE, acute post-streptococcal glomerulonephritis, membranoproliferative glomerulonephritis, chronic liver disease. Increased: Seen in acute inflammation, early infection. |
| C4 | A key component of both the classical and lectin pathways. | Decreased: Has relatively high specificity for SLE; also seen in hereditary angioedema (C1 esterase inhibitor deficiency), cryoglobulinemia. |
| C5 | The starting component for Membrane Attack Complex (MAC) formation; generates the potent inflammatory mediator C5a. | Decreased: Associated with recurrent infections and autoimmune diseases. C5a is a major chemoattractant involved in intense inflammatory responses. |
| C6 | A MAC assembly component. | Decreased: Primarily linked to recurrent infections with Neisseria meningitidis, suggesting a terminal complement component deficiency. |
| C7 | A MAC assembly component. | Decreased: Also associated with increased susceptibility to Neisseria meningitidis or Neisseria gonorrhoeae. |
| C9 | The terminal component of MAC, enhancing its lytic efficiency. | Decreased: Deficiency may be asymptomatic in some populations; severe deficiency can increase infection risk. |
Service Advantages
Our service strength lies in providing professional and precise quantitative analysis of the complement system. Leveraging a reliable detection platform, we enable accurate quantification of multiple complement proteins—from initiators (C1q) to terminal components (C9)—helping you comprehensively assess the functional status of all three activation pathways. We go beyond providing data on individual components by emphasizing the correlated interpretation of key indicators like C3, C4, and C1q, offering deeper insights into disease activity and potential defect points. Standardized operations and stringent quality control throughout the process ensure stable and reliable results. With a standard turnaround time of approximately one week, we efficiently support your clinical and research needs.
Workflow
You communicate with our technical support team to clarify the required panel of complement components and sample details.
Following the provided guidelines, collect non-anticoagulated peripheral blood (to obtain serum) or prepare serum samples. Ship them to the laboratory under cold-chain conditions (2-8°C) using sufficient ice packs.
The laboratory receives the samples, verifies information, and performs quality checks (e.g., for hemolysis, lipemia). Qualified samples undergo preprocessing for testing.
Processed samples are analyzed using specialized instrumentation for quantitative complement component analysis, generating raw concentration data.
Data is analyzed and calculated. A preliminary report is created using reference ranges and undergoes review before the final version is issued.
The formal electronic test report is sent to you, accompanied by the availability of professional consultation for result interpretation.
Notes
- Sample Requirements: Serum separated from non-anticoagulated peripheral blood is recommended. Samples should be free from severe hemolysis (as lysed red blood cells release substances that can interfere with complement activity). Freshly separated serum can be stored at 2-8°C for 1-3 days.
- Long-term Storage Protocol: For long-term storage, aliquot the serum and immediately freeze it at -80°C, strictly avoiding repeated freeze-thaw cycles to prevent denaturation and degradation of complement proteins.
- Result Interpretation: Complement levels are influenced by various factors. Slight fluctuations in a single indicator require comprehensive evaluation alongside clinical symptoms and other immune markers (e.g., autoantibodies, immunoglobulins). The report will provide reference ranges and brief guidance.
