Review
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World J Clin Infect Dis. Aug 25, 2013; 3(3): 37-46
Published online Aug 25, 2013. doi: 10.5495/wjcid.v3.i3.37
Physiological functions and clinical implications of fibrinogen-like 2: A review
Genyan Yang, W Craig Hooper
Genyan Yang, W Craig Hooper, Clinical and Molecular Hemostasis Laboratory Branch, Division of Blood Disorders, National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, Atlanta, GA 30301, United States
Author contributions: Yang G and Hooper WC contributed to this paper.
Correspondence to: W Craig Hooper, PhD, Clinical and Molecular Hemostasis Laboratory Branch, Division of Blood Disorders, National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, 1600 Clifton Road, N.E., Atlanta, GA 30329, United States. chooper@cdc.gov
Telephone: +1-404-6393570 Fax: +1-404-6391638
Received: June 28, 2013
Revised: July 23, 2013
Accepted: August 16, 2013
Published online: August 25, 2013
Processing time: 69 Days and 2.9 Hours
Core Tip

Core tip: Fibrinogen-like 2 (FGL2) protein promotes coagulation as a prothrombinase, or acts as an immunosuppressor to repress function of T lymphocytes and dendritic cells and induce apoptosis of B lymphocytes. Ectopic expression of FGL2 has been proven relevant for the pathogenesis of viral infections. Induction of FGL2 in response to pathogen invasion causes focal prothrombin activation and fibrin deposition. This process may lead to inflammation, microvascular thrombosis, and subsequent organ failure. FGL2-mediated immunosuppression can facilitate pathogen proliferation and expansion. The understanding of FGL2-mediated pathophysiology offers an insight into biomarker development and clinical intervention of FGL2-associated medical conditions such as viral hepatitis.