FcRn Produits

FcRn enhances IgG immune response: The neonatal Fc receptor (FcRn) enhances the distinct roles that IgGs play in the adaptive immune response, e.g. when protecting the body from infection. Specifically interaction between IgGs and FcRn lead to high IgG circulating levels, long IgG half-life, and the ability of IgGs to transfer from mother to offspring.

FcRn protects IgG from degradation and facilitates transport: FcRn binds to the Fc portion of IgGs in a pH-dependent manner, protecting IgGs from intracellular degradation. It facilitates the transport of IgGs across polarized cells, like endothelium and epithelium, and potentiates cellular immune responses when IgGs form immune complexes with antigens.

FcRn blockade to reduce IgG autoantibodies: IgG autoantibodies are associated with numerous pathological conditions. Consequently, FcRn blockade has emerged as a novel strategy to reduce circulating levels of pathogenic IgG autoantibodies and manage IgG-mediated diseases.

FcRn plays a significant role in the metabolism of albumin: Albumin is the most abundant protein in the blood plasma and serves multiple functions, including maintaining osmotic pressure, binding and transporting various molecules, and serving as a reservoir of amino acids. FcRn binding is crucial for protecting albumin from lysosomal degradation. Furthermore FcRn regulates the serum half-life of albumin. By recycling albumin back into the bloodstream and preventing its catabolism, FcRn helps maintain stable serum albumin levels.

FcRn is expressed across various cell types: FcRn is expressed in various haematopoietic cell types, particularly in myeloid cells like monocytes, macrophages, dendritic cells, and neutrophils. Its expression is also noted in B cells, but not in T cells or NK cells. FcRn is mostly found intracellularly in acidic endosomes, facilitating interactions with IgG and albumin, and is also present on the cell surface in some cells.

FcRn expression is influenced by factors like cytokines and infectious stimuli: For instance, TNF stimulation increases FcRn expression in certain cell lines, dependent on NF-κB binding. Toll-like receptor agonists and transforming growth factor β1 also upregulate FcRn expression through various pathways. Conversely, interferon-γ can downregulate FcRn expression through JAK-STAT1 signalling.