About this Research Topic
This Research Topic is the second volume of "The Role of Complement in Health and Disease" Community Series. Please see volume I here.
The complement system is a crucial mediator of the innate immune response, interacting with other innate mechanisms and with factors of acquired immunity. It contributes significantly to cell homeostasis, tissue development and repair, reproduction, and cross-talk with other endogenous cascades. Each of the three major complement activation pathways (Classical, CP; Alternative, AP and Lectin, LP) employs specific recognition molecules and initiating serine proteases. All of them converge into a common pathway, leading to the formation of the biologically highly active anaphylatoxin C5a and the C5b-9 membrane attack complex (MAC). The latter forms transmembrane channels which either induce “sub-lytic” activation of the cell or result in target cell lysis. Although the complement system was discovered in 1888, nowadays this system is still under intense investigation with ongoing advances being made in various aspects including its clinical significance and its involvement in the regulation of the immune response.
Generally, as an important branch of first-line defense, complement protects the host from invading pathogens and abnormal self-derived components. This can be achieved through several mechanisms: (i) opsonization by activated factors, (ii) by attracting immune cells and enhancing phagocytosis or (iii) by direct lysis after incorporation of the MAC into the cell envelope of the invading pathogen. Therefore, complement plays key roles in (i) preventing the spread of infection to other cells and tissues, (ii) participating in the clearance of damaged cells and tissues, and (iii) preventing the development of chronic inflammation and/or cancer. On the other hand, uncontrolled complement activation may lead to life-threatening effects such as systemic inflammation and shock, dysregulation of coagulation/fibrinolysis, and auto-aggression. Furthermore, under certain conditions, deregulated complement activation may also promote tumorigenesis.
This Research Topic aims to summarize recent achievements in the field of complement research. We welcome the submission of Original Research articles presenting basic and/or translational studies as well as Review, Mini-Review, and Systematic Review articles focused on, but not limited to, the following topics:
1. Basic knowledge concerning CP, AP, and LP: their activation, regulation, and specific receptors.
2. Cross-talk of complement with other endogenous signaling cascades.
3. Genetics of complement (including animal models).
4. Clinical aspects of deregulated complement activation and deficiencies: infections/sepsis, cancer, and auto-aggression (including animal models).
5. Complement in therapy or its therapeutic inhibition.
The complement system is a crucial mediator of the innate immune response, interacting with other innate mechanisms and with factors of acquired immunity. It contributes significantly to cell homeostasis, tissue development and repair, reproduction, and cross-talk with other endogenous cascades. Each of the three major complement activation pathways (Classical, CP; Alternative, AP and Lectin, LP) employs specific recognition molecules and initiating serine proteases. All of them converge into a common pathway, leading to the formation of the biologically highly active anaphylatoxin C5a and the C5b-9 membrane attack complex (MAC). The latter forms transmembrane channels which either induce “sub-lytic” activation of the cell or result in target cell lysis. Although the complement system was discovered in 1888, nowadays this system is still under intense investigation with ongoing advances being made in various aspects including its clinical significance and its involvement in the regulation of the immune response.
Generally, as an important branch of first-line defense, complement protects the host from invading pathogens and abnormal self-derived components. This can be achieved through several mechanisms: (i) opsonization by activated factors, (ii) by attracting immune cells and enhancing phagocytosis or (iii) by direct lysis after incorporation of the MAC into the cell envelope of the invading pathogen. Therefore, complement plays key roles in (i) preventing the spread of infection to other cells and tissues, (ii) participating in the clearance of damaged cells and tissues, and (iii) preventing the development of chronic inflammation and/or cancer. On the other hand, uncontrolled complement activation may lead to life-threatening effects such as systemic inflammation and shock, dysregulation of coagulation/fibrinolysis, and auto-aggression. Furthermore, under certain conditions, deregulated complement activation may also promote tumorigenesis.
This Research Topic aims to summarize recent achievements in the field of complement research. We welcome the submission of Original Research articles presenting basic and/or translational studies as well as Review, Mini-Review, and Systematic Review articles focused on, but not limited to, the following topics:
1. Basic knowledge concerning CP, AP, and LP: their activation, regulation, and specific receptors.
2. Cross-talk of complement with other endogenous signaling cascades.
3. Genetics of complement (including animal models).
4. Clinical aspects of deregulated complement activation and deficiencies: infections/sepsis, cancer, and auto-aggression (including animal models).
5. Complement in therapy or its therapeutic inhibition.
Keywords: Complement, Membrane attack complex, Innate Immune Response
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
