The 155-KDa glycoprotein complement factor H (FH) was first described in 1965 and soon emerged as a major soluble inhibitor of the complement system. While other fluid-phase and cell membrane-bound regulators of complement have been identified, FH is essential for controlling complement activation on various ...
The 155-KDa glycoprotein complement factor H (FH) was first described in 1965 and soon emerged as a major soluble inhibitor of the complement system. While other fluid-phase and cell membrane-bound regulators of complement have been identified, FH is essential for controlling complement activation on various cellular and non-cellular surfaces, including basement membranes. Several studies reported links between genetic variations of FH and disease, thus confirming the important role of FH in the regulation of complement activation. Moreover, numerous pathogenic microbes and some tumor cells have developed the ability to exploit FH for complement evasion. In addition to its canonical role in complement regulation, several other functions of FH have been discovered and a large number of binding partners have been identified. Factor H-like 1 (FHL-1) is a splice variant of FH that also possesses complement-inhibiting function. Additional five factor H-related (FHR) proteins belong to the FH family and have been recognized as competitors of FH for binding to various ligands, thus modulating complement regulation.
The aim of this Research Topic is to provide insights into the physiological roles of FH, its ligands and mechanisms of action, and the pathological consequences of its malfunctioning, or misappropriation by harmful cells. We will achieve this aim by assembling a set of both fundamental and clinically oriented research articles. We welcome Original Research, Review, Mini-Review, Case Report and Perspective articles related to the following themes:
1. Structure-function studies of FH.
2. Roles of FH in diseases, based on genetic, experimental and/or clinical data.
3. FH in complement evasion by microbes or tumor cells.
4. The use of animal models to explore FH function in health and disease and the treatment of diseases linked to FH dysfunction.
5. Modulation of FH functions by ligands or via competition by e.g. FHR proteins.
6. Non-canonical roles of FH.
Topic Editor Dr. Barlow is a founder of Gemini Therapeutics. The other Topic Editors declare no competing interests with regards to the Research Topic theme
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.