The complement system is a key innate immune system and contributes to the control of pathogens from the very beginning of an infection, before the generation of antibodies. Its function is to clear invading microbes by either forming a membrane-attack complex on the surface of the invader, or by marking these with complement C3 split products (opsonization), and attracting and activating immune cells. Both mechanisms markedly support phagocytosis by macrophages and dendritic cells. Thus, the complement system bridges the innate with the adaptive immune system.
Specific proteins can sense invading microbes and trigger one of the three main complement pathways. I) The classical pathway (CP) is activated by immune complexes, pentraxins (C-reactive protein and pentraxin 3) or by direct interaction of C1 with the surface of pathogens. II) Initiation of the lectin pathway (LP) is mediated by MBL, ficolins (ficolin-1, ficolin-2, and ficolin-3), or collectins (collectin-10 and collectin-11) binding to glycosylated or acetylated residues on the envelope of the invading microorganism. III) Spontaneous hydrolysis of a labile thioester bond converts C3 to a bioactive form C3(H2O) and keeps the alternative pathway (AP) constitutively active at low-levels in the plasma. Independently of the pathway, complement activation converges to the terminal pathway resulting in the generation of the membrane attack complex.
Over millions of years, pathogens such as bacteria, viruses, fungi or parasites have learned to evade the action of complement either in a passive way to protect themselves or in an aggressive way to enter host cells and maintain infection.
The aim of this Research Topic is to better describe the complement-dependent mechanisms designed to destroy pathogens, alongside a more detailed characterization of complement evasion strategies of pathogens. It is clear that both actions influence each other and are interwoven. We welcome authors to submit Original Research and Review articles focusing on, but not limited to, the following subtopics:
1. Complement mediated mechanisms for pathogen clearing
2. Complement evasion strategies evolved from pathogens, including mimicry or acquisition of complement regulatory proteins
3. Complement-medicated enhancement of infection
The complement system is a key innate immune system and contributes to the control of pathogens from the very beginning of an infection, before the generation of antibodies. Its function is to clear invading microbes by either forming a membrane-attack complex on the surface of the invader, or by marking these with complement C3 split products (opsonization), and attracting and activating immune cells. Both mechanisms markedly support phagocytosis by macrophages and dendritic cells. Thus, the complement system bridges the innate with the adaptive immune system.
Specific proteins can sense invading microbes and trigger one of the three main complement pathways. I) The classical pathway (CP) is activated by immune complexes, pentraxins (C-reactive protein and pentraxin 3) or by direct interaction of C1 with the surface of pathogens. II) Initiation of the lectin pathway (LP) is mediated by MBL, ficolins (ficolin-1, ficolin-2, and ficolin-3), or collectins (collectin-10 and collectin-11) binding to glycosylated or acetylated residues on the envelope of the invading microorganism. III) Spontaneous hydrolysis of a labile thioester bond converts C3 to a bioactive form C3(H2O) and keeps the alternative pathway (AP) constitutively active at low-levels in the plasma. Independently of the pathway, complement activation converges to the terminal pathway resulting in the generation of the membrane attack complex.
Over millions of years, pathogens such as bacteria, viruses, fungi or parasites have learned to evade the action of complement either in a passive way to protect themselves or in an aggressive way to enter host cells and maintain infection.
The aim of this Research Topic is to better describe the complement-dependent mechanisms designed to destroy pathogens, alongside a more detailed characterization of complement evasion strategies of pathogens. It is clear that both actions influence each other and are interwoven. We welcome authors to submit Original Research and Review articles focusing on, but not limited to, the following subtopics:
1. Complement mediated mechanisms for pathogen clearing
2. Complement evasion strategies evolved from pathogens, including mimicry or acquisition of complement regulatory proteins
3. Complement-medicated enhancement of infection
