C1Q- complement | Laboratory research

General Information

The complement system is part of the immune system and is involved in the removal of microbes and damaged cells. It functions together with antibodies and phagocytes to form the complement cascade, as cascade reactions are triggered when complement is activated. The complement system is the front line of immunity in the fight against pathogens.

The c1q component of complement is a protein with a molecular weight of 400 kDa, which consists of three molecules, C1q, C1r and C1s, which are non-covalently linked to each other and to Ca2+ ions. c1q globular domain interacts with specific domains of IgG and IgM and forms immune complexes. C1q has no protease activity.

After the formation of the antigen-antibody complex, c1q undergoes a conformational change, which leads to the removal of the c1-inhibitor (blocking) protein and the activation of the c1r molecule.

Such molecules as: c-reactive protein, β-amyloid, heparin, some gram-negative bacteria, viruses, mycoplasmas, cellular components - DNA, mitochondrial membrane, cytoskeleton filaments and others, also have the ability to activate complement.

Congenital deficiency of c1-c4 components of complement leads to failure of peptides required for removal of immune complexes, attraction of neutrophils to the center and initiation of catalytic activity. Such patients are at high risk of infections with encapsulated microorganisms and may also develop an autoimmune disease.

When is the survey conducted?

C1 To diagnose complement deficiency

Preparation of the patient: The study is conducted on an empty stomach.

Material for examination: Venous blood

Referral norm: 160 – 310 mg/l

Interpretation of results

Low levels of complement components indicate acquired, congenital deficiencies, or excessive absorption of complement as a result of autoimmune diseases.

Hereditary complement C1 deficiency is rare. Its deficiency is associated with diseases characterized by the formation of immune complexes, such as: systemic lupus erythematosus, polymyositis, glomerulonephritis and Schönlein-Henoch purpura.

Systemic lupus erythematosus is most commonly characterized by c1 complement deficiency. The clinical manifestation of the disease does not correlate with the degree of complement deficiency.

A low level of C1 complement also characterizes conditions with an abnormal titer of immunoglobulins (Bruton's hypogammaglobulinemia, acute immunodeficiency, etc.).

The level of complement proteins in the serum increases against the background of inflammatory and infectious processes. After the end of the pathological process, the indicators are normalized.