{"id":1146,"date":"2017-01-02T08:30:05","date_gmt":"2017-01-02T07:30:05","guid":{"rendered":"https:\/\/newscientific.eu\/c1q\/"},"modified":"2025-05-15T11:39:57","modified_gmt":"2025-05-15T09:39:57","slug":"c1q","status":"publish","type":"page","link":"https:\/\/newscientific.eu\/en\/c1q\/","title":{"rendered":"C1q"},"content":{"rendered":"
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C1q<\/h2>\n

C1q is a 480 kDa protein involved in the classical pathway of the complement cascade of the immunitary system contributing to the innate defence against infections.
\nBinding its targets, such as antigen-bound immunoglobulins or C-reactive protein, C1q leads to the release of inflammation stimulating peptides, C3a and C5a, to the formation of the opsonin C3b and to the formation of the membrane attack complex, resulting in target cell lysis. Furthermore, C1q is involved in phagocytosis or myeloid cell modulation and its circulating levels are determined in routine diagnostics as biomarker in several disease.
\nDecreased C1q levels are observed in some autoimmune conditions (such as Systemic lupus erythematosus (SLE), hypocomplementemic urticaria vasculitis syndrome, angioedema) and reflect the consumption of C1q by complement activation. For this reason, its quantification is useful as a marker for disease activity.
\nInstead, the increase of C1q levels in serum suggest the negative modulation of the adaptive immune response as C1q is well know to impact on the maturation status of antigen-presenting cells leading to decrease T-cell activity. High levels of C1q can be observed related to infectious and inflammatory disease (tuberculosis, sarcoidosis, leprosy, malaria) (1).<\/p>\n

Reference<\/em><\/p>\n