protein_function: Secreted protein that acts as a key regulator of lipidsynthesis: mainly expressed by macrophages in lymphoid andinflammed tissues and regulates mechanisms in inflammatoryresponses, such as infection or atherosclerosis. Able to inhibitlipid droplet size in adipocytes. Following incorporation intomature adipocytes via CD36-mediated endocytosis, associates withcytosolic FASN, inhibiting fatty acid synthase activity andleading to lipolysis, the degradation of triacylglycerols intoglycerol and free fatty acids (FFA). CD5L-induced lipolysis occurswith progression of obesity: participates to obesity-associatedinflammation following recruitment of inflammatory macrophagesinto adipose tissues, a cause of insulin resistance and obesity-related metabolic disease. Regulation of intracellular lipidsmediated by CD5L has a direct effect on transcription regulationmediated by nuclear receptors ROR-gamma (RORC). Acts as a keyregulator of metabolic switch in T-helper Th17 cells. Regulatesthe expression of pro-inflammatory genes in Th17 cells by alteringthe lipid content and limiting synthesis of cholesterol ligand ofRORC, the master transcription factor of Th17-celldifferentiation. CD5L is mainly present in non-pathogenic Th17cells, where it decreases the content of polyunsaturated fattyacyls (PUFA), affecting two metabolic proteins MSMO1 and CYP51A1,which synthesize ligands of RORC, limiting RORC activity andexpression of pro-inflammatory genes. Participates in obesity-associated autoimmunity via its association with IgM, interferingwith the binding of IgM to Fcalpha,mu receptor and enhancing thedevelopment of long-lived plasma cells that produce high-affinityIgG autoantibodies (By similarity). Also acts as an inhibitor ofapoptosis in macrophages: promotes macrophage survival from theapoptotic effects of oxidized lipids in case of atherosclerosis(PubMed:24295828). Involved in early response to microbialinfection against various pathogens by acting as a patternrecognition receptor and by promoting autophagy (PubMed:16030018,PubMed:24223991, PubMed:24583716, PubMed:25713983)..
CD5 antigen-like, also known as Sp alpha and AIM, is a protein that in humans is encoded by the CD5L gene. It is mapped to 1q21-q23 by fluorescence in situ hybridization. It is found that Aim expression is induced in mouse macrophages in response to loading with highly oxidized low density lipoprotein (oxLDL), and that Aim is expressed in foam cells within atherosclerotic lesions. Both the expression of Aim in lesions and its induction by oxLDL require Lxr ,Rxr heterodimers. Aim-null macrophages are highly susceptible to oxLDL-induced apoptosis in vitro and undergo accelerated apoptosis in atherosclerotic lesions in vivo. Double knockout of Aim and Ldlr reduce atherosclerotic lesions. Therefore, it is concluded that AIM expression protects macrophages from apoptosis within atherosclerotic lesions, promoting early lesion development.