The role of the complement system in dermatological disease

References

• Walport MJ. Complement. First of two parts. N. Engl. J. Med. 344(14), 1058–1066 (2001).
   PubMed Web of Science ®Google Scholar
• Walport MJ. Complement. Second of two parts. N. Engl. J. Med. 344(15), 1140–1144 (2001).
   PubMed Web of Science ®Google Scholar
• Zipfel PF, Würzner R, Skerka C. Complement evasion of pathogens: common strategies are shared by diverse organisms. Mol. Immunol. 44(16), 3850–3857 (2007).
   PubMed Web of Science ®Google Scholar
• Flierman R, Daha MR. The clearance of apoptotic cells by complement. Immunobiology 212(4–5), 363–370 (2007).
   PubMedGoogle Scholar
• Ogden CA, Elkon KB. Role of complement and other innate immune mechanisms in the removal of apoptotic cells. Curr. Dir. Autoimmun. 9, 120–142 (2006).
   PubMedGoogle Scholar
• Trouw LA, Blom AM, Gasque P. Role of complement and complement regulators in the removal of apoptotic cells. Mol. Immunol. 45(5), 1199–1207 (2008).
   PubMed Web of Science ®Google Scholar
• Ricklin D, Hajishengallis G, Yang K, Lambris JD. Complement: a key system for immune surveillance and homeostasis. Nat. Immunol. 11(9), 785–797 (2010).
   PubMed Web of Science ®Google Scholar
• Pangburn MK, Schreiber RD, Müller-Eberhard HJ. Formation of the initial C3 convertase of the alternative complement pathway. Acquisition of C3b-like activities by spontaneous hydrolysis of the putative thioester in native C3. J. Exp. Med. 154(3), 856–867 (1981).
   PubMed Web of Science ®Google Scholar
• Pangburn MK, Schreiber RD, Müller-Eberhard HJ. Formation of the initial C3 convertase of the alternative complement pathway. Acquisition of C3b-like activities by spontaneous hydrolysis of the putative thioester in native C3. J. Exp. Med. 154(3), 856–867 (1981).
   PubMed Web of Science ®Google Scholar
• Fujita T. Evolution of the lectin-complement pathway and its role in innate immunity. Nat. Rev. Immunol. 2(5), 346–353 (2002).
   PubMed Web of Science ®Google Scholar
• Degn SE, Thiel S, Jensenius JC. New perspectives on mannan-binding lectin-mediated complement activation. Immunobiology 212(4–5), 301–311 (2007).
   PubMedGoogle Scholar
• Daha NA, Banda NK, Roos A et al. Complement activation by (auto-) antibodies. Mol. Immunol. 48(14), 1656–1665 (2011).
   PubMed Web of Science ®Google Scholar
• Wallis R, Mitchell DA, Schmid R, Schwaeble WJ, Keeble AH. Paths reunited: initiation of the classical and lectin pathways of complement activation. Immunobiology 215(1), 1–11 (2010).
   PubMed Web of Science ®Google Scholar
• Osthoff M, Trendelenburg G, Eisen DP, Trendelenburg M. Mannose-binding lectin – the forgotten molecule? Nat. Med. 17(12), 1547–1548; author reply 1548 (2011).
   PubMedGoogle Scholar
• Garred P, Larsen F, Seyfarth J, Fujita R, Madsen HO. Mannose-binding lectin and its genetic variants. Genes Immun. 7(2), 85–94 (2006).
   PubMed Web of Science ®Google Scholar
• Spitzer D, Mitchell LM, Atkinson JP, Hourcade DE. Properdin can initiate complement activation by binding specific target surfaces and providing a platform for de novo convertase assembly. J. Immunol. 179(4), 2600–2608 (2007).
   PubMed Web of Science ®Google Scholar
• Fearon DT, Austen KF. Properdin: binding to C3b and stabilization of the C3b-dependent C3 convertase. J. Exp. Med. 142(4), 856–863 (1975).
   PubMedGoogle Scholar
• Xu W, Berger SP, Trouw LA et al. Properdin binds to late apoptotic and necrotic cells independently of C3b and regulates alternative pathway complement activation. J. Immunol. 180(11), 7613–7621 (2008).
   PubMedGoogle Scholar
• Sjöberg AP, Trouw LA, Blom AM. Complement activation and inhibition: a delicate balance. Trends Immunol. 30(2), 83–90 (2009).
   PubMed Web of Science ®Google Scholar
• Degn SE, Jensenius JC, Thiel S. Disease-causing mutations in genes of the complement system. Am. J. Hum. Genet. 88(6), 689–705 (2011).
   PubMed Web of Science ®Google Scholar
• Yang Y, Chung EK, Wu YL et al. Gene copy-number variation and associated polymorphisms of complement component C4 in human systemic lupus erythematosus (SLE): low copy number is a risk factor for and high copy number is a protective factor against SLE susceptibility in European Americans. Am. J. Hum. Genet. 80(6), 1037–1054 (2007).
   PubMed Web of Science ®Google Scholar
• Wu YL, Yang Y, Chung EK et al. Phenotypes, genotypes and disease susceptibility associated with gene copy number variations: complement C4 CNVs in European American healthy subjects and those with systemic lupus erythematosus. Cytogenet. Genome Res. 123(1–4), 131–141 (2008).
   PubMed Web of Science ®Google Scholar
• Jamal S, Jolles S. The role of complement testing in dermatology. Clin. Exp. Dermatol. 30(4), 321–326 (2005).
   PubMedGoogle Scholar
• Rook’s Textbook of Dermatology. Burns T, Breathnach S, Cox N, Griffiths C (Eds). Wiley-Blackwell, Oxford, UK (2010).
   Google Scholar
• Trouw LA, Roos A, Daha MR. Autoantibodies to complement components. Mol. Immunol. 38(2–3), 199–206 (2001).
   PubMed Web of Science ®Google Scholar
• Zuraw BL. Clinical practice. Hereditary angioedema. N. Engl. J. Med. 359(10), 1027–1036 (2008).
   PubMed Web of Science ®Google Scholar
• Lawrence CP. Hereditary angioedema: diagnosis and management – a perspective for the dermatologist. J. Am. Acad. Dermatol. 65(4), 843–850 (2011).
   PubMedGoogle Scholar
• Waytes AT, Rosen FS, Frank MM. Treatment of hereditary angioedema with a vapor-heated C1 inhibitor concentrate. N. Engl. J. Med. 334(25), 1630–1634 (1996).
   PubMed Web of Science ®Google Scholar
• Bork K, Barnstedt SE. Treatment of 193 episodes of laryngeal edema with C1 inhibitor concentrate in patients with hereditary angioedema. Arch. Intern. Med. 161(5), 714–718 (2001).
   PubMed Web of Science ®Google Scholar
• Cicardi M, Banerji A, Bracho F et al. Icatibant, a new bradykinin-receptor antagonist, in hereditary angioedema. N. Engl. J. Med. 363(6), 532–541 (2010).
   PubMed Web of Science ®Google Scholar
• Cugno M, Zanichelli A, Bellatorre AG, Griffini S, Cicardi M. Plasma biomarkers of acute attacks in patients with angioedema due to C1-inhibitor deficiency. Allergy 64(2), 254–257 (2009).
   PubMedGoogle Scholar
• Karim Y, Griffiths H, Deacock S. Normal complement C4 values do not exclude hereditary angioedema. J. Clin. Pathol. 57(2), 213–214 (2004).
   PubMed Web of Science ®Google Scholar
• Bork K, Barnstedt SE, Koch P, Traupe H. Hereditary angioedema with normal C1-inhibitor activity in women. Lancet 356(9225), 213–217 (2000).
   PubMed Web of Science ®Google Scholar
• Binkley KE, Davis A 3rd. Clinical, biochemical, and genetic characterization of a novel estrogen-dependent inherited form of angioedema. J. Allergy Clin. Immunol. 106(3), 546–550 (2000).
   PubMed Web of Science ®Google Scholar
• Cichon S, Martin L, Hennies HC et al. Increased activity of coagulation factor XII (Hageman factor) causes hereditary angioedema type III. Am. J. Hum. Genet. 79(6), 1098–1104 (2006).
   PubMed Web of Science ®Google Scholar
• Mehregan D . Dermatological Manifestations of Urticarial Vasculitis. Elston DM (Ed.). Medscape, NY, USA (2010).
   Google Scholar
• Cees GMK. Anti-C1q autoantibodies. Autoimmun. Rev. 7(8), 612–615 (2008).
   PubMedGoogle Scholar
• Seelen MA, Trouw LA, Daha MR. Diagnostic and prognostic significance of anti-C1q antibodies in systemic lupus erythematosus. Curr. Opin. Nephrol. Hypertens. 12(6), 619–624 (2003).
   PubMed Web of Science ®Google Scholar
• Pickering MC, Botto M, Taylor PR, Lachmann PJ, Walport MJ. Systemic lupus erythematosus, complement deficiency, and apoptosis. Adv. Immunol. 76, 227–324 (2000).
   PubMed Web of Science ®Google Scholar
• Lipsker D, Hauptmann G. Cutaneous manifestations of complement deficiencies. Lupus 19(9), 1096–1106 (2010).
   PubMedGoogle Scholar
• Truedsson L, Bengtsson AA, Sturfelt G. Complement deficiencies and systemic lupus erythematosus. Autoimmunity 40(8), 560–566 (2007).
   PubMed Web of Science ®Google Scholar
• Lawley TJ, Bielory L, Gascon P, Yancey KB, Young NS, Frank MM. A study of human serum sickness. J. Invest. Dermatol. 85(Suppl. 1), 129s–132s (1985).
   PubMed Web of Science ®Google Scholar
• Lawley TJ, Bielory L, Gascon P, Yancey KB, Young NS, Frank MM. A prospective clinical and immunologic analysis of patients with serum sickness. N. Engl. J. Med. 311(22), 1407–1413 (1984).
   PubMed Web of Science ®Google Scholar
• Bielory L, Yancey KB, Young NS, Frank MM, Lawley TJ. Cutaneous manifestations of serum sickness in patients receiving antithymocyte globulin. J. Am. Acad. Dermatol. 13(3), 411–417 (1985).
   PubMed Web of Science ®Google Scholar
• Hebert AA, Sigman ES, Levy ML. Serum sickness-like reactions from cefaclor in children. J. Am. Acad. Dermatol. 25(5 Pt 1), 805–808 (1991).
   PubMedGoogle Scholar
• Martin J, Abbott G. Serum sickness like illness and antimicrobials in children. NZ Med. J. 108(997), 123–124 (1995).
   PubMedGoogle Scholar
• King BA, Geelhoed GC. Adverse skin and joint reactions associated with oral antibiotics in children: the role of cefaclor in serum sickness-like reactions. J. Paediatr. Child Health 39(9), 677–681 (2003).
   PubMed Web of Science ®Google Scholar
• Brouet JC, Clauvel JP, Danon F, Klein M, Seligmann M. Biologic and clinical significance of cryoglobulins. A report of 86 cases. Am. J. Med. 57(5), 775–788 (1974).
   PubMed Web of Science ®Google Scholar
• Ferri C, Zignego AL, Pileri SA. Cryoglobulins. J. Clin. Pathol. 55(1), 4–13 (2002).
   PubMed Web of Science ®Google Scholar
• Ferri C, Mascia MT. Cryoglobulinemic vasculitis. Curr. Opin. Rheumatol. 18(1), 54–63 (2006).
   PubMed Web of Science ®Google Scholar
• Sansonno D, Dammacco F. Hepatitis C virus, cryoglobulinaemia, and vasculitis: immune complex relations. Lancet Infect. Dis. 5(4), 227–236 (2005).
   PubMed Web of Science ®Google Scholar
• Ramos-Casals M, Stone JH, Cid MC, Bosch X. The cryoglobulinaemias. Lancet 379(9813), 348–360 (2012).
   PubMed Web of Science ®Google Scholar
• Ferri C, Sebastiani M, Giuggioli D et al. Mixed cryoglobulinemia: demographic, clinical, and serologic features and survival in 231 patients. Semin. Arthritis Rheum. 33(6), 355–374 (2004).
   PubMed Web of Science ®Google Scholar
• Ramos-Casals M, Stone JH, Cid MC, Bosch X. The cryoglobulinaemias. Lancet 379(9813), 348–360 (2012).
   PubMed Web of Science ®Google Scholar
• Trendelenburg M, Hess C, Kondo-Oestreicher M, Tissot JD, Späth P, Schifferli JA. Monomeric complement-activating IgG paraproteins. J. Immunol. 163(12), 6924–6932 (1999).
   PubMedGoogle Scholar
• Jones RR. Cutaneous manifestations of paraproteinaemia. Part II. Br. J. Dermatol. 104(2), 209–220 (1981).
   PubMedGoogle Scholar
• Naish PF, Collins C, Barratt J. Classical pathway complement activation in association with paraproteinaemia. Immunology 33(4), 517–521 (1977).
   PubMedGoogle Scholar
• Kondo-Oestreicher M, Chizzolini C, Tissot JD et al. Hypocomplementemic panniculitis with paraprotein. J. Rheumatol. 27(4), 1091–1095 (2000).
   PubMedGoogle Scholar
• Wojnarowska F, Kirtschig G, Highet AS, Venning VA, Khumalo NP; British Association of Dermatologists. Guidelines for the management of bullous pemphigoid. Br. J. Dermatol. 147(2), 214–221 (2002).
   PubMed Web of Science ®Google Scholar
• Jordon RE, Kawana S, Fritz KA. Immunopathologic mechanisms in pemphigus and bullous pemphigoid. J. Invest. Dermatol. 85(Suppl. 1), 72s–78s (1985).
   Google Scholar
• Jordon RE. Complement activation in bullous skin diseases. J. Invest. Dermatol. 65(1), 162–169 (1975).
   PubMedGoogle Scholar
• Chorzelski TP, Cormane RH. The presence of complement “bound” in vivo in the skin of patients with pemphigoid. Dermatologica 137(3), 134–138 (1968).
   PubMedGoogle Scholar
• Lessey E, Li N, Diaz L, Liu Z. Complement and cutaneous autoimmune blistering diseases. Immunol. Res. 41(3), 223–232 (2008).
   PubMed Web of Science ®Google Scholar
• Liu Z, Giudice GJ, Swartz SJ et al. The role of complement in experimental bullous pemphigoid. J. Clin. Invest. 95(4), 1539–1544 (1995).
   PubMed Web of Science ®Google Scholar
• Nelson KC, Zhao M, Schroeder PR et al. Role of different pathways of the complement cascade in experimental bullous pemphigoid. J. Clin. Invest. 116(11), 2892–2900 (2006).
   PubMed Web of Science ®Google Scholar
• Mooney E, Falk RJ, Gammon WR. Studies on complement deposits in epidermolysis bullosa acquisita and bullous pemphigoid. Arch. Dermatol. 128(1), 58–60 (1992).
   PubMedGoogle Scholar
• Smoller BR, Woodley DT. Differences in direct immunofluorescence staining patterns in epidermolysis bullosa acquisita and bullous pemphigoid. J. Am. Acad. Dermatol. 27(5 Pt 1), 674–678 (1992).
   PubMedGoogle Scholar
• Cho HJ, Lee IJ, Kim SC. Complement-fixing abilities and IgG subclasses of autoantibodies in epidermolysis bullosa acquisita. Yonsei Med. J. 39(4), 339–344 (1998).
   PubMedGoogle Scholar
• Mihai S, Chiriac MT, Takahashi K et al. The alternative pathway of complement activation is critical for blister induction in experimental epidermolysis bullosa acquisita. J. Immunol. 178(10), 6514–6521 (2007).
   PubMed Web of Science ®Google Scholar
• Nousari HC, Anhalt GJ. Pemphigus and bullous pemphigoid. Lancet 354(9179), 667–672 (1999).
   PubMed Web of Science ®Google Scholar
• Daha MR, Fearon DT, Austen KF. C3 nephritic factor (C3NeF): stabilization of fluid phase and cell-bound alternative pathway convertase. J. Immunol. 116(1), 1–7 (1976).
   PubMed Web of Science ®Google Scholar
• Walport MJ, Davies KA, Botto M et al. C3 nephritic factor and SLE: report of four cases and review of the literature. QJM 87(10), 609–615 (1994).
   PubMedGoogle Scholar
• Gompels MM, Lock RJ, Morgan JE, Osborne J, Brown A, Virgo PF. A multicentre evaluation of the diagnostic efficiency of serological investigations for C1 inhibitor deficiency. J. Clin. Pathol. 55(2), 145–147 (2002).
   PubMedGoogle Scholar
• Tarzi MD, Hickey A, Förster T, Mohammadi M, Longhurst HJ. An evaluation of tests used for the diagnosis and monitoring of C1 inhibitor deficiency: normal serum C4 does not exclude hereditary angio-oedema. Clin. Exp. Immunol. 149(3), 513–516 (2007).
   PubMed Web of Science ®Google Scholar
• Seelen MA, Roos A, Wieslander J et al. Functional analysis of the classical, alternative, and MBL pathways of the complement system: standardization and validation of a simple ELISA. J. Immunol. Methods 296(1–2), 187–198 (2005).
   PubMed Web of Science ®Google Scholar
• Sullivan KE, Petri MA, Schmeckpeper BJ, McLean RH, Winkelstein JA. Prevalence of a mutation causing C2 deficiency in systemic lupus erythematosus. J. Rheumatol. 21(6), 1128–1133 (1994).
   PubMed Web of Science ®Google Scholar
• Davila S, Wright VJ, Khor CC et al.; International Meningococcal Genetics Consortium. Genome-wide association study identifies variants in the CFH region associated with host susceptibility to meningococcal disease. Nat. Genet. 42(9), 772–776 (2010).
   PubMed Web of Science ®Google Scholar
• Kuijpers TW, Nguyen M, Hopman CT et al. Complement factor 7 gene mutations in relation to meningococcal infection and clinical recurrence of meningococcal disease. Mol. Immunol. 47(4), 671–677 (2010).
   PubMedGoogle Scholar