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 induces “sub-lytic” activation of the cell, or results in target cell lysis. Although the complement system was discovered in 1888, nowadays this system is still under intense investigation with on-going 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.
The aim of this Research Topic is 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, LP: their activation, regulation, 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 induces “sub-lytic” activation of the cell, or results in target cell lysis. Although the complement system was discovered in 1888, nowadays this system is still under intense investigation with on-going 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.
The aim of this Research Topic is 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, LP: their activation, regulation, 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.
