Factor H (FH) is a member of the regulators of complement activation family and is a complement control protein. It is a large (155 kilodaltons), soluble glycoprotein that circulates in human plasma (at typical concentrations of 200–300 micrograms per milliliter[5][6][7]). Its principal function is to regulate the alternative pathway of the complement system, ensuring that the complement system is directed towards pathogens or other dangerous material and does not damage host tissue. Factor H regulates complement activation on self cells and surfaces by possessing both cofactor activity for Factor I–mediated C3b cleavage, and decay accelerating activity against the alternative pathway C3-convertase, C3bBb. Factor H exerts its protective action on self cells and self surfaces but not on the surfaces of bacteria or viruses. There are however, important exceptions, such as for example the bacterial pathogen, Neisseria meningitidis (also called the meningococcus). This human pathogen has evolved mechanisms to recruit human FH and down-regulate the alternative pathway.[8] Binding of FH permits the bacteria to proliferate in the bloodstream and cause disease.[9]
The ability of Factor H to exert its protective action on self cells and self surfaces is thought to be the result of Factor H having the ability to adopt conformations with lower or higher activities as a cofactor for C3 cleavage or decay accelerating activity.[10] The lower activity conformation is the predominant form in solution and is sufficient to control fluid phase amplification. The more active conformation is thought to be induced when Factor H binds to glycosaminoglycans (GAGs) and or sialic acids that are generally present on host cells but not, normally, on pathogen surfaces ensuring that self surfaces are protected whilst complement fixation proceeds unabated on foreign surfaces.[11][12]
^ abcGRCh38: Ensembl release 89: ENSG00000000971 – Ensembl, May 2017
^ abcGRCm38: Ensembl release 89: ENSMUSG00000026365 – Ensembl, May 2017
^"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
^Sofat R, Mangione PP, Gallimore JR, Hakobyan S, Hughes TR, Shah T, et al. (April 2013). "Distribution and determinants of circulating complement factor H concentration determined by a high-throughput immunonephelometric assay". Journal of Immunological Methods. 390 (1–2): 63–73. doi:10.1016/j.jim.2013.01.009. PMID 23376722.
^Hakobyan S, Harris CL, Tortajada A, Goicochea de Jorge E, García-Layana A, Fernández-Robredo P, et al. (May 2008). "Measurement of factor H variants in plasma using variant-specific monoclonal antibodies: application to assessing risk of age-related macular degeneration". Investigative Ophthalmology & Visual Science. 49 (5): 1983–1990. doi:10.1167/iovs.07-1523. hdl:10261/56608. PMID 18436830.
^Scholl HP, Charbel Issa P, Walier M, Janzer S, Pollok-Kopp B, Börncke F, et al. (July 2008). "Systemic complement activation in age-related macular degeneration". PLOS ONE. 3 (7): e2593. Bibcode:2008PLoSO...3.2593S. doi:10.1371/journal.pone.0002593. PMC 2440421. PMID 18596911.
^Lewis LA, Carter M, Ram S (May 2012). "The relative roles of factor H binding protein, neisserial surface protein A, and lipooligosaccharide sialylation in regulation of the alternative pathway of complement on meningococci". Journal of Immunology. 188 (10): 5063–5072. doi:10.4049/jimmunol.1103748. PMC 3345070. PMID 22504643.
^Vu DM, Shaughnessy J, Lewis LA, Ram S, Rice PA, Granoff DM (February 2012). Bliska JB (ed.). "Enhanced bacteremia in human factor H transgenic rats infected by Neisseria meningitidis". Infection and Immunity. 80 (2): 643–650. doi:10.1128/IAI.05604-11. PMC 3264313. PMID 22104107.
^Herbert AP, Makou E, Chen ZA, Kerr H, Richards A, Rappsilber J, Barlow PN (November 2015). "Complement Evasion Mediated by Enhancement of Captured Factor H: Implications for Protection of Self-Surfaces from Complement". Journal of Immunology. 195 (10): 4986–4998. doi:10.4049/jimmunol.1501388. PMC 4635569. PMID 26459349.
^Pangburn MK (August 2000). "Host recognition and target differentiation by factor H, a regulator of the alternative pathway of complement". Immunopharmacology. 49 (1–2): 149–157. doi:10.1016/S0162-3109(00)80300-8. PMID 10904114.
^Rodríguez de Córdoba S, Esparza-Gordillo J, Goicoechea de Jorge E, Lopez-Trascasa M, Sánchez-Corral P (June 2004). "The human complement factor H: functional roles, genetic variations and disease associations". Molecular Immunology. 41 (4): 355–367. doi:10.1016/j.molimm.2004.02.005. PMID 15163532.
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