Discrimination between host and pathogens by the complement system.
Pathogen-specific complement activation requires direct recognition of pathogens and/or the absence of complement control mechanisms on their surfaces. Antibodies direct complement activation to potential pathogens recognized by the cellular innate and adaptive immune systems. Similarly, the plasma proteins MBL and ficolins direct activation to microorganisms expressing common carbohydrate structures. The absence of complement control proteins permits amplification of complement by the alternative pathway on any unprotected surface. The importance of complement recognition molecules (MBL, ficolins, factor H, C3, C1q, properdin, and others) to human disease are becoming clear as analysis of genetic data and knock out animals reveals links between complement proteins and specific diseases.
Pangburn
Michael K
MK
Department of Biochemistry, Center for Biomedical Research, University of Texas Health Science Center, Tyler, TX 75708, USA. michael.pangburn@uthct.edu
Ferreira
Viviana P
VP
Cortes
Claudio
C
D000818:Animals; D018958:CD55 Antigens / Q000502:physiology; D018957:CD59 Antigens / Q000502:physiology; D003167:Complement Activation; D003165:Complement System Proteins / Q000502:physiology*; D054884:Host-Pathogen Interactions; D006801:Humans; D007113:Immunity, Innate; D037102:Lectins / Q000502:physiology; D008268:Macular Degeneration / Q000209:etiology
D018958:CD55 Antigens; D018957:CD59 Antigens; D037102:Lectins; C051590:CD59 protein, human; D003165:Complement System Proteins