» Articles » PMID: 20580090

Complement Control Protein Factor H: the Good, the Bad, and the Inadequate

Overview
Journal Mol Immunol
Date 2010 Jun 29
PMID 20580090
Citations 201
Authors
Affiliations
Soon will be listed here.
Abstract

The complement system is an essential component of the innate immune system that participates in elimination of pathogens and altered host cells and comprises an essential link between the innate and adaptive immune system. Soluble and membrane-bound complement regulators protect cells and tissues from unintended complement-mediated injury. Complement factor H is a soluble complement regulator essential for controlling the alternative pathway in blood and on cell surfaces. Normal recognition of self-cell markers (i.e. polyanions) and C3b/C3d fragments is necessary for factor H function. Inadequate recognition of host cell surfaces by factor H due to mutations and polymorphisms have been associated with complement-mediated tissue damage and disease. On the other hand, unwanted recognition of pathogens and altered self-cells (i.e. cancer) by factor H is used as an immune evasion strategy. This review will focus on the current knowledge related to these versatile recognition properties of factor H.

Citing Articles

HTRA1 and complement activation in neovascular age-related macular degeneration.

Tanaka K, Omori T, Oguchi Y, Itagaki K, Kato Y, Honjo J Jpn J Ophthalmol. 2025; .

PMID: 39937341 DOI: 10.1007/s10384-024-01153-4.


Tissue origin of endothelial cells determines immune system modulation and regulation of HIF-1α-, TGF-β-, and VEGF signaling.

Heiden R, Hannig L, Bernhard J, Vallon M, Schlecht A, Hofmann N iScience. 2025; 28(2):111740.

PMID: 39925414 PMC: 11804623. DOI: 10.1016/j.isci.2024.111740.


Survival of Strain B31 in Human Serum Is Not Dependent on C4BP Binding to the Bacterial Surface.

Jakobsson T, Comstedt P, Bergstrom S, Normark J Pathogens. 2024; 13(11).

PMID: 39599529 PMC: 11597344. DOI: 10.3390/pathogens13110976.


The Complement Factor H (Y402H) risk polymorphism for age-related macular degeneration affects metabolism and response to oxidative stress in the retinal pigment epithelium.

Shang P, Ambrosino H, Hoang J, Geng Z, Zhu X, Shen S Free Radic Biol Med. 2024; 225():833-845.

PMID: 39491736 PMC: 11662989. DOI: 10.1016/j.freeradbiomed.2024.10.307.


Glomerular injury induced by vinyl carbamate in A/J inbred mice: a novel model of membranoproliferative glomerulonephritis.

Gong A, Qiao Y, Chen M, Alam Z, Malhotra D, Dworkin L Front Pharmacol. 2024; 15:1462936.

PMID: 39309006 PMC: 11412833. DOI: 10.3389/fphar.2024.1462936.


References
1.
Klickstein L, Wong W, Smith J, Weis J, Wilson J, Fearon D . Human C3b/C4b receptor (CR1). Demonstration of long homologous repeating domains that are composed of the short consensus repeats characteristics of C3/C4 binding proteins. J Exp Med. 1987; 165(4):1095-112. PMC: 2188588. DOI: 10.1084/jem.165.4.1095. View

2.
Meri T, Jokiranta T, Hellwage J, Bialonski A, Zipfel P, Meri S . Onchocerca volvulus microfilariae avoid complement attack by direct binding of factor H. J Infect Dis. 2002; 185(12):1786-93. DOI: 10.1086/340649. View

3.
MULLER-EBERHARD H, Gotze O . C3 proactivator convertase and its mode of action. J Exp Med. 1972; 135(4):1003-8. PMC: 2139164. DOI: 10.1084/jem.135.4.1003. View

4.
Thurman J, Renner B, Kunchithapautham K, Ferreira V, Pangburn M, Ablonczy Z . Oxidative stress renders retinal pigment epithelial cells susceptible to complement-mediated injury. J Biol Chem. 2009; 284(25):16939-16947. PMC: 2719331. DOI: 10.1074/jbc.M808166200. View

5.
Sahu A, Pangburn M . Covalent attachment of human complement C3 to IgG. Identification of the amino acid residue involved in ester linkage formation. J Biol Chem. 1994; 269(46):28997-9002. View