Ficolin

Source: Wikipedia, the free encyclopedia.

Ficolins are

complement cascade.[1]

Structure

Ficolins (Fi+Col+Lin) are a group of oligomeric lectins with N-terminal collagen-like domain and a C-terminal fibrinogen-like domain. The primary ficolin structure contains 288 amino acids. The combination of collagen-like and fibrinogen-like domain allows the protein to form a basic subunit containing a triple helical tail and a trio of globular heads.[2]

Ficolins are produced in the liver by hepatocytes and in the lung by alveolar cells type II, neutrophils and monocytes.[3]

Role in innate immunity

We now know that innate immune recognition mechanisms are sophisticated. Exocrine secretions provide a variety of soluble factors that are able to protect the body from potential pathogens.[4]

Together with

mannose-binding protein-associated serine proteases (MASPs) that ficolins are associated to and co-circulate with.[1][6] Serine proteases then cleave a number of soluble complement proteins leading to complement activation, opsonisation, generation of proinflammatory mediators, and cell lysis.[7]

Collectins and ficolins are also called collagenous lectins. The collectin family constitutes calcium-dependent proteins. In contrast, the ficolin family does not bind to PAMPs in a calcium-dependent way.[3]

Types of ficolin

Three ficolins have been identified in humans:

  1. M-ficolin (FCN1), monocyte ficolin
  2. L-ficolin (FCN2), liver ficolin
  3. H-ficolin (FCN3), hakata antigen.[2][3]

Ficolin-1 and ficolin-2 are encoded be a gene localised on chromosome 9 (9q34) and they share approximately 80% identity in amino sequence. Whereas, ficolin-3 is encoded by chromosome 1 and therefore it has only about 50% identity with the other two ficolins.[2] A cross-reactivity of the ficolins in human serum has been observed.[7]

Clinical references

The concentration of ficolins in healthy serum is between 3 and 5 μg/mL.[2]

As Ficolin-2 and 3 are expressed by hepatocytes, their levels decrease in advanced liver diseases like cirrhosis. Low ficolin levels contribute to cirrhosis-associated immune dysfunction.[8]

Immunologist Jeak L. Ding and her team found that natural IgG (nIgG; a non-specific immunoglobulin of adaptive immunity) is not quiescent, but plays a crucial role in immediate immune defense by collaborating with ficolin (an innate immune protein).[9]

References