The complement activation product C5a interacts not only with PMN via abundantly expressed specific receptors (C5aR1 = CD88 and C5aR2 = C5L2
= GPR77) [5, 6] but also with other immune cells and epithelial cells .
The C5-like receptor 2 (C5L2) is postulated to be a unique ASP receptor, although some studies found no interaction between C5L2 and ASP (19, 25).
In addition, abnormal keratinocyte proliferation is a characteristic of psoriasis, and the lack of C5L2 expression on epidermal keratinocytes may explain the low ASP level in the patient group.
In 2000 and 2001, the human C5aR2 gene (also named GPR77 or C5L2, C5a-like receptor 2) was cloned by two independent research groups [10, 11].
Takahashi, "A putative chemoattractant receptor, C5L2, is expressed in granulocyte and immature dendritic cells, but not in mature dendritic cells," Molecular Immunology, vol.
These complement components bind to a family of three receptors, which belong to the superfamily of G-protein-coupled receptors: the C3a receptor (C3aR), C5a receptor (C5aR), and C5a receptor-like 2 (C5L2).
C5L2 binds C5a as well as C5adesArg, the latter with a higher affinity than to C5aR .
It was revealed that septic patients had low expression levels of C5aR and C5L2
on neutrophils compared to healthy and SIRS cases, and this expression pattern was correlated with disease severity.[sup]
C3a and C5a exert these proinflammatory effects by binding to their respective receptors, C3a receptor (C3aR), and the two receptors for C5, C5a receptor (C5aR; CD88) and C5a receptor-like 2 receptor (C5L2
ASP manifests its insulin-like effects on differentiated human adipocytes via the receptor C5L2 .
C5L2, initially proposed as a nonfunctional receptor, has been shown to be actively involved in inflammatory conditions such as insulin resistance, asthma, and coronary artery disease [14,15].
ASP acts through its only known receptor, C5L2
. This 7-transmembrane receptor is widely expressed, with expression in tissues such as liver, muscle, adipose tissue, immune cells, and brain, and C5L2
shares significant homology with other complement receptors such as C3a receptor and C5a receptor .