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C1 inhibitor: from complement system to bradykinin angioedema
Federica Defendi1, Axelle Amen2, Giovanna Clavarino2
1Univ. Grenoble Alpes, CHU Grenoble Alpes, Laboratoire d'Immunologie, 38000 Grenoble, France.
Current Opinion in Immunology
|September 4, 2025
Summary
C1 Inhibitor (C1INH) deficiency causes bradykinin-mediated angioedema (AE). Diagnosis relies on C1INH levels and function, with research exploring new markers and comorbidities.
Area of Science:
- Biochemistry
- Immunology
- Genetics
Background:
- C1 Inhibitor (C1INH) regulates complement, coagulation, kallikrein-kinin, and fibrinolysis pathways.
- C1INH deficiency leads to bradykinin (BK) overproduction, causing angioedema (AE).
- AE is a rare disease marked by unpredictable swelling attacks.
Purpose of the Study:
- To summarize current understanding of C1INH deficiency and AE.
- To highlight diagnostic standards and emerging AE types.
- To outline research directions in BK-mediated angioedema.
Main Methods:
- Review of C1INH function and deficiency mechanisms.
- Analysis of diagnostic criteria for hereditary and acquired AE.
- Examination of recent guidelines and research trends.
Main Results:
- C1INH deficiency is a primary cause of AE, linked to BK.
- Hereditary and acquired forms of C1INH deficiency exist, with specific diagnostic markers.
- New forms of hereditary angioedema with normal C1INH activity have been identified.
Conclusions:
- C1INH level and functional assays are key for AE diagnosis.
- Updated guidelines address AE classification, diagnosis, and management.
- Future research focuses on novel biomarkers and C1INH deficiency comorbidities.
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