Sandwich ELISA, Biotin-labelled antibody
At ambient temperature. Upon receipt, store the product at the temperature recommended below.
Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).
Limit of Detection
n = 8; CV = 3.6%
n = 5; CV = 6.1%
- For research use only!
- The total assay time is less than 4 hours
- The kit measures total AIM in serum and plasma (heparin)
- Assay format is 96 wells
- Standard is recombinant protein
- Components of the kit are provided ready to use, concentrated or lyophilized
Cardiovascular disease, Immune Response, Infection and Inflammation, Metabolic syndrome, Renal disease
CD5 molecule-like protein (CD5L), also known as apoptosis inhibitor expressed by macrophages (AIM), is a 50 kDa alternative cell surface ligand for CD5, a glycoprotein expressed on T lymphocytes. It is a soluble glycosylated protein that belongs to group B scavenger receptor cysteine-rich (SRCR) superfamily. Its expression was detected in the macrophages present in several lymphoid tissues. It is widely known, that oxLDL is an inducer of AIM expression. Biochemical studies of this molecule revealed that it is an abundant serum protein and might play a role in the homeostasis of IgM antibodies, because CD5L was found to circulate in serum mostly in complex with IgM. CD5L has been demonstrated to support the survival of macrophages and enhanced the phagocytic function of macrophages. In mice, it was also shown to inhibit the apoptosis of NKT cells and T cells. CD5L is up-regulated in macrophages at inflammatory sites. Increased level of CD5L protects foam cells from apoptosis but permits more rapid cellular accumulation and atherosclerotic plaque formation.
AIM is incorporated into adipocytes via endocytosis mediated by the CD 36 scavenger receptor and induces lipolysis via the reduction of FAS enzymatic activity. This decreases lipid droplet storage within adipocytes and their size. On the other hand, when this lipolytic effect is excessive, it triggers chronic inflammation via the recruitment of macrophages into adipose tissue, leading to insulin resistance (IR). During early periods of MetS AIM can help prevent the progression of obesity through lipolysis; in obese conditions, anti-AIM therapy should prevent the development of metabolic diseases such as diabetes and cardiovascular events. One of the criteria for assessing whether AIM or anti-AIM therapy should be administered is the blood AIM level.
As written above, most of circulating AIM is associated with IgM pentamers. A strong correlation between AIM and natural IgM levels in the blood has been found in both humans and mice. Accordingly, the serum level of AIM was far lower in mice lacking blood IgM and the level of AIM rapidly increased after intravenous injection of monoclonal mouse IgM. The complex formation maintains the blood AIM level at a relatively high concentration (about 10μg/ml). A large proportion of natural IgM is polyreactive to not only foreign antigens but also autoantigens, including nucleic acids, heat shock proteins, carbohydrates, and phospholipids. Thus, IgM is believed to be important for the progression of autoimunity.
One of the main diseases underlying chronic kidney disease (CKD) is nephrosclerosis, which involves progressive arteriosclerosis at the level of small arteries and arterioles in the kidneys leading to ischemic changes in the glomeruli and interstitium, consequently compromising renal function. As was previously reported, macrophages play a major role in the progression of arteriosclerosis. Uramatsu and co. showed that AIM expression in macrophages in the renal tissue of stroke-prone spontaneously hypertensive (SHRsp) rats seemed closely correlated with the number of infiltrating macrophages. It is well known that glomerular or interstitial macrophage infiltration is a prominent feature in nephrosclerosis, diabetic nephropathy, and lupus nephritis.