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Apoptosis Inhibitor of Macrophage Human ELISA

  • Regulatory status:RUO
  • Type:Sandwich ELISA, Biotin-labelled antibody
  • Other names:CD5 molecul-like protein
  • Species:Human
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Cat. No. Size Price


RD191328200R 96 wells (1 kit)
PubMed Product Details
Technical Data

Type

Sandwich ELISA, Biotin-labelled antibody

Applications

Serum, Plasma-Heparin

Sample Requirements

10 ul/wel

Storage/Expiration

Store the complete kit at 2–8°C. Under these conditions, the kit is stable until the expiration date (see label on the box).

Calibration Range

0.16–10.0 ng/mL

Limit of Detection

0.009 ng/mL

Intra-assay (Within-Run)

n = 8; CV = 3.6%

Inter-assay (Run-to-Run)

n = 5; CV = 6.1%

Spiking Recovery

99,70%

Dilutation Linearity

103,30%

Summary

Features

  • 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

Research topic

Cardiovascular disease, Immune Response, Infection and Inflammation, Metabolic syndrome, Renal disease

Summary

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.

References to Summary

References to Apoptosis Inhibitor of Macrophage

  • Arai S, Miyazaki T. Impacts of the apoptosis inhibitor of macrophage (AIM) on obesity-associated inflammatory diseases. Semin Immunopathol. 2014 Jan;36 (1):3-12
  • Arai S, Shelton JM, Chen M, Bradley MN, Castrillo A, Bookout AL, Mak PA, Edwards PA, Mangelsdorf DJ, Tontonoz P, Miyazaki T. A role for the apoptosis inhibitory factor AIM/Spalpha/Api6 in atherosclerosis development. Cell Metab. 2005 Mar;1 (3):201-13
  • Boes M. Role of natural and immune IgM antibodies in immune responses. Mol Immunol. 2000 Dec;37 (18):1141-9
  • Calvo J, Places L, Padilla O, Vila JM, Vives J, Bowen MA, Lozano F. Interaction of recombinant and natural soluble CD5 forms with an alternative cell surface ligand. Eur J Immunol. 1999 Jul;29 (7):2119-29
  • Gebe JA, Kiener PA, Ring HZ, Li X, Francke U, Aruffo A. Molecular cloning, mapping to human chromosome 1 q21-q23, and cell binding characteristics of Spalpha, a new member of the scavenger receptor cysteine-rich (SRCR) family of proteins. J Biol Chem. 1997 Mar 7;272 (10):6151-8
  • Hardy RR, Hayakawa K. CD5 B cells, a fetal B cell lineage. Adv Immunol. 1994;55:297-339
  • Haruta I, Kato Y, Hashimoto E, Minjares C, Kennedy S, Uto H, Yamauchi K, Kobayashi M, Yusa S, Muller U, Hayashi N, Miyazaki T. Association of AIM, a novel apoptosis inhibitory factor, with hepatitis via supporting macrophage survival and enhancing phagocytotic function of macrophages. J Biol Chem. 2001 Jun 22;276 (25):22910-4
  • Kuwata K, Watanabe H, Jiang SY, Yamamoto T, Tomiyama-Miyaji C, Abo T, Miyazaki T, Naito M. AIM inhibits apoptosis of T cells and NKT cells in Corynebacterium-induced granuloma formation in mice. Am J Pathol. 2003 Mar;162 (3):837-47
  • Mimura I, Nangaku M. The suffocating kidney: tubulointerstitial hypoxia in end-stage renal disease. Nat Rev Nephrol. 2010 Nov;6 (11):667-78
  • Miyazaki T, Kurokawa J, Arai S. AIMing at metabolic syndrome. -Towards the development of novel therapies for metabolic diseases via apoptosis inhibitor of macrophage (AIM).-. Circ J. 2011;75 (11):2522-31
  • Nakaya H, Sasamura H, Hayashi M, Saruta T. Temporary treatment of prepubescent rats with angiotensin inhibitors suppresses the development of hypertensive nephrosclerosis. J Am Soc Nephrol. 2001 Apr;12 (4):659-66
  • Sarrias MR, Padilla O, Monreal Y, Carrascal M, Abian J, Vives J, Yelamos J, Lozano F. Biochemical characterization of recombinant and circulating human Spalpha. Tissue Antigens. 2004 Apr;63 (4):335-44
  • Tissot JD, Sanchez JC, Vuadens F, Scherl A, Schifferli JA, Hochstrasser DF, Schneider P, Duchosal MA. IgM are associated to Sp alpha (CD5 antigen-like). Electrophoresis. 2002 Apr;23 (7-8):1203-6
  • Uramatsu T, Nishino T, Obata Y, Sato Y, Furusu A, Koji T, Miyazaki T, Kohno S. Involvement of apoptosis inhibitor of macrophages in a rat hypertension model with nephrosclerosis: possible mechanisms of action of olmesartan and azelnidipine. Biol Pharm Bull. 2013;36 (8):1271-7
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