This receptor contains two alternative splice variants (SR-BI and SR-BII), and contrary to CD36 receptor, SR-BI recognizes mainly HDL and is responsible for reverse cholesterol transport; however it also recognizes altered lipids, among them oxLDL, as well as native LDL, suggesting that SR-BI could play a role in normal LDL metabolism  and could present a selective lipid uptake from HDL [91, 92]. SR-BI is expressed in different tissues such as adrenal glands, steroidogenic tissue and hepatocytes, as well as Mangiferin in different types of cells, like monocytes, macrophages and dendritic cells . that B cell can recognize/remove lipids through a range of receptors, such as LDLR, CD1d, FcR and SR, which might have an atheroprotector or proatherogenic role during the course of atherosclerotic disease. Relevant literature related to these receptors was examined to inform the present conclusions. mice, showing Mangiferin an atherogenic effect [35, 36]. B lymphocytes express a variety of receptors that identify foreign, endogenous or modified self-antigens, among them oxidized low density lipoproteins (oxLDL), which are the main antigens in PLA2G10 atherosclerosis. B cell mechanisms to recognize, remove and present lipids are not completely obvious. However, it has been reported that B cells can remove lipid antigens through a B cell receptor (BCR) dependent via, but also there is internalization and antigen presentation to invariant natural killer T (iNKT) cells by BCR impartial via, associated to low density lipoprotein receptor (LDLR) expression on activated B cells [37C41]. CD1 is included among the receptors expressed in B cells that have the ability to present lipid antigens. They belong to 2 microglobulin family associated polypeptides, which relate with the major histocompatibility complex (MHC) class I and II. Also, B cells express Fc receptors (FcR), which through their immunoreceptor tyrosine-based activation or inhibitory motifs (ITAMs or ITIMs) initiate and propagate early signaling events leading to cell-specific responses , and scavenger receptors (SR), which belong to the Mangiferin family of pattern acknowledgement receptors (PRR), that identify pathogen associated molecular patterns (PAMPs), as well as altered antigens, such as death associated molecular patterns (DAMPs), including altered host derived molecules like oxLDL [43, 44] (Table?1). Table 1 Receptors involved in lipid recognition-removal or presentation and immune responses in experimental atherosclerotic disease mice fed a high excess fat diet.Undetermined[58, 59]FcRIIBDeficiency in the chain expression of FcR in mice, which approximately developed just a 20% of lesion assessed by analysis of whole aortas, compared with control mice.Proatherogenic[85C87]Triple knockout mice, exhibited increased serum cholesterol levels and larger atherosclerotic lesions located in aortic sinus compared with mice as controls, suggesting that SR mediated lipid uptake protected against atherosclerosis lesion formation rather than promote it.AtheroprotectorAortic lesion analysis in mice fed with western diet and mice revealed no difference between the groups, however bone marrow transplant from mice had 38.4% less lesion area compared with those receiving transplant.ProatherogenicSR-BI mice fed with standard chow diet designed occlusive coronary artery atherosclerosis as well as significant atherosclerotic lesions, compared with control mice.Atheroprotector[95C97]Transplantation of bone marrow Mangiferin from mice into mice present a 50% reduction in lesion formation compared with controls, but the influence on lesion progression is just transient and does not Mangiferin significantly impact the inflammatory cytokine milieu of mature lesions.Proatherogenic[118C120] Open in a separate windows The disruption of cellular homeostasis through oxidative stress and contribution to cell death by generation of harmful intermediates during aberrant lipid metabolism, and enhanced pro-inflammatory immunological pathways, could occur in vascular, cardiac and adipose tissue diseases. This opens up the possibility that immune cells often interacting with oxidized products, and more specifically B cells, could participate in the process of lipotoxicity at the hurt areas during the tissue remodeling process, leading to development and establishment of the disease or even regulating the inflammatory process. This supports the importance of understanding the receptors that could be involved in lipids acknowledgement and/or removal by B cells. Receptors involved in lipids recognition-removal by B cells LDLR Lymphocytes obtain cholesterol from serum low density lipoproteins (LDL) through its specific LDLR, which is usually internalized along with LDL; since these cells do not synthetize enough cholesterol to support their membranes [45C47]. The main function of this mechanism is usually to transfer cholesterol from plasma LDL into the cell in a controlled manner . LDL endocytosis and subsequent lysosomal degradation induces the release of free cholesterol, which suppresses 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA) activity, stimulates acyl-CoA cholesterol acyltransferase (ACAT) and regulates the LDLR activity by a opinions mechanism [49, 50]. LDLR is usually widely expressed in different cell types, including T and B lymphocytes . However there are important differences in cholesterol metabolism among these lymphocyte subpopulations;.