Ficolin-3

Background

Ficolin-3, also named H-ficolin, is a plasma protein first discovered in 1990 as an autoantigen. It is a soluble pattern recognition molecule (PRM) of the innate immune system and binds to acetylated molecules, for example, as found in acetylated carbohydrate structures or on proteins via its fibrinogen-like recognition domain. The fitting patterns recognized by ficolin-3 may be present on apoptotic and necrotic cells, and this offers ficolin-3 the possibility of acting as an initiator of scavenging actions. Besides, ficolin-3 plays an important role in the complement system which can activate the lectin pathway (LP), causing both anti-microbial defense and homeostatic balance. To initiate this activation, ficolin-3 relies on the activation of attached enzymes, i.e., so-called Mannose-binding lectin (MBL)-associated serine proteases (MASPs). When compared to ficolin-1, ficolin-2, MBL, and collectin-LK, ficolin-3 is the most abundant of the five PRMs of the LP.

Research showed that a frameshift mutation in exon 5 (FCN3 + 1637delC) of the FCN3 gene, resulting in premature termination of transcription was demonstrated to be involved in lower levels of ficolin-3 in the heterozygous state. It also revealed that ficolin-3 participate in the clearance of dying host cells. Furthermore, ficolin-3 deficiency is a rare condition and is related to both infection and autoimmune disease including systemic lupus erythematosus (SLE). A study has proven that ficolin-3 deficiency causes an 8-time increased odds of having a disease (p<0.05).

Fig. 1 Structure of H-ficolin.^{1, 3}

Ficolin-3 Functional Service

Creative Biolabs provides a broad array of ficolin-3-focused supplies, encompassing anti-ficolin-3 antibodies, ELISA kits, and human complement ficolin-3 proteins. These meticulously designed tools are essential in propelling research initiatives aimed at formulating therapeutic approaches for various diseases.

Fig.2 Activity of ficolin-3 in Individuals with systemic lupus erythematosus.^{2, 3}

Researchers targeted the lectin pathway to elucidate its role in Systemic Lupus Erythematosus (SLE), highlighting ficolin-3 as a focal point due to its predominant role in complement activation. They assessed ficolin-3 activity in Swedish SLE patients and controls, finding that higher ficolin-3 activity significantly correlated with a cluster characterized by specific antibodies and increased lymphopenia and hematological disease rates. Genetic analysis revealed that low ficolin-3 activity linked to variants near the FCN3 gene reduced the frequency of these manifestations and autoantibodies. Although FCN3 gene loss-of-function variants weren’t linked to SLE broadly, a subset showed acquired ficolin-3 deficiency post-diagnosis, underscoring ficolin-3’s role in modulating disease pathways.

Creative Biolabs presents a wide selection of ficolin-3-related services, comprising binding evaluations and supplementary functional analyses, meticulously customized to aid their distinguished clients in clinical and research pursuits.

References

1. Mason, Christopher P., and Alexander W. Tarr. "Human lectins and their roles in viral infections." Molecules 20.2 (2015): 2229-2271.
2. Lindelöf, Linnea, et al. "A survey of ficolin-3 activity in Systemic Lupus Erythematosus reveals a link to hematological disease manifestations and autoantibody profile." Journal of Autoimmunity 143 (2024): 103166.
3. Distributed under Open Access license CC BY 4.0, without modification.