Table 1 Receptors involved in lipid recognition-removal or presentation and immune responses in experimental atherosclerotic disease

Receptors involved in lipids recognition-removal or presentation by B cells

LDLR

Internalization of LDL through LDLR, to transfer cholesterol from plasma LDL into the cell in a controlled manner.

A defect in the expression or internalization of LDLR leads to an increase in circulating plasma LDL, predisposing them to oxidation, condition that contributes in a great manner to the physiopathology of atherosclerosis.

Undetermined

[54, 55]

FcR

Recognition of immunoglobulins directed to modified lipids, more specifically neoepitopes formed by lipid peroxidation.

FcμR

High titers of anti-oxLDL IgM in Apoe ^−/− mice fed a high fat diet.

Undetermined

[58, 59]

FcγRIIB

Deficiency in the γ chain expression of FcγR in Apoe ^−/−mice fed with high fat diet, is related with a limited development and progression of atherosclerosis that could be associated with the loss of FcγRI and FcγRIIIA, and the overexpression of the inhibitory FcγRIIB characteristic of this mouse model.

Atheroprotector

[69, 70]

Absence of FcγRIIB induces increased atherosclerosis development in Ldlr ^−/−atherosclerosis mouse model, as well as increased activation and expansion of B cells.

Undetermined

[71]

The absence of FcγRIIB induces increased atherosclerosis development in Ldlr ^−/−atherosclerosis mouse model, as well as increased activation and expansion of B cells.

[72]

SR

Recognition of several ligands, such as microbial, environmental, endogenous and self-modified antigens, either by endocytosis or phagocytosis, contributing to the outcome of the immune system responses.

CD36

The absence of CD36 protects against atherosclerotic lesion development in Apoe ^−/− mice, which approximately developed just a 20% of lesion assessed by en face analysis of whole aortas, compared with control mice.

Proatherogenic

[85–87]

Triple knockout CD36 ^−/− Msr1 ^−/− Apoe ^−/− mice, exhibited increased serum cholesterol levels and larger atherosclerotic lesions located in aortic sinus compared with Apoe ^−/− mice as controls, suggesting that SR mediated lipid uptake protected against atherosclerosis lesion formation rather than promote it.

Atheroprotector

[88]

Aortic lesion analysis in Ldlr ^−/− CD36 ^−/− mice fed with western diet and Ldlr ^−/− mice revealed no difference between the groups, however bone marrow transplant from Ldlr-CD36 ^−/−into Apoe ^−/− mice had 38.4% less lesion area compared with those receiving Ldlr ^−/− transplant.

Proatherogenic

[89]

SR-BI

SRBI ^−/− Apoe ^−/− mice fed with standard chow diet developed occlusive coronary artery atherosclerosis as well as significant atherosclerotic lesions, compared with control mice.

Atheroprotector

[95–97]

Transplantation of bone marrow from SR-BI ^−/− mice into Ldlr ^−/−mice, induced a twofold reduction of the mean atherosclerotic lesion area after 4 weeks of high fat diet.

Proatherogenic

[98]

CD1

Presentation of lipid antigens or hydrophobic peptide antigens to T cells, activating a specialized T cell subset called invariant NKT cells (iNKT), and leading to immune responses that contribute with the inflammatory process.

CD1d

CD1d ^−/− Ldlr ^−/− mice present a 50% reduction in lesion formation compared with controls, but the influence on lesion progression is just transient and does not significantly affect the inflammatory cytokine milieu of mature lesions.

Proatherogenic

[118–120]