Formyl peptide receptor 3

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Formyl Peptide Receptor 3 (FPR3) is a G protein-coupled receptor (GPCR) that belongs to the formyl peptide receptor family. It plays a crucial role in the immune system by mediating chemotaxis of neutrophils and other immune cells towards sites of inflammation or infection. FPR3 is activated by formyl peptides, which are short sequences of amino acids that can be derived from both bacterial sources and mitochondrial proteins released during cell damage.

Structure and Function[edit | edit source]

FPR3, like other members of the GPCR family, spans the cell membrane seven times. This receptor is predominantly expressed in immune cells, including neutrophils, monocytes, and dendritic cells. Upon activation by its ligands, FPR3 initiates a signaling cascade through the associated G proteins, leading to various cellular responses such as chemotaxis, degranulation, and the production of reactive oxygen species.

The ligands for FPR3 are diverse and include formyl peptides from bacteria and mitochondria, as well as other non-formylated peptides. This diversity in ligand recognition allows FPR3 to respond to a wide range of inflammatory signals.

Role in Immunity[edit | edit source]

FPR3 plays a significant role in the innate immune response by directing immune cells to sites of infection or tissue damage. Its ability to mediate chemotaxis is crucial for the rapid recruitment of neutrophils and other immune cells, which are essential for the initial defense against pathogens and for the clearance of damaged cells.

In addition to its role in chemotaxis, FPR3 signaling can also influence the expression of cytokines and other inflammatory mediators, further modulating the immune response.

Clinical Significance[edit | edit source]

Alterations in FPR3 expression or function have been implicated in various inflammatory diseases and conditions. Overactivation of FPR3 signaling can contribute to excessive inflammation, leading to tissue damage in diseases such as rheumatoid arthritis, asthma, and sepsis. Conversely, impaired FPR3 function can result in inadequate immune responses, increasing susceptibility to infections.

Given its role in inflammation and immunity, FPR3 is a potential target for therapeutic interventions. Modulating FPR3 activity could offer new approaches for treating inflammatory diseases, either by inhibiting excessive immune responses or by enhancing immune responses when necessary.

Research Directions[edit | edit source]

Research on FPR3 is ongoing, with studies aimed at better understanding its signaling mechanisms, ligand specificity, and role in various diseases. Developing specific agonists and antagonists for FPR3 could provide valuable tools for dissecting its functions and for therapeutic applications.

See Also[edit | edit source]

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Contributors: Prab R. Tumpati, MD