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Target Concepts:
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Query: UMLS:C0004153 (
atherosclerosis
)
77,401
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Mast cells (MCs) are potent innate immune cells that aggravate
atherosclerosis
through the release of proinflammatory mediators inside atherosclerotic plaques. Similarly, CD4
+
T cells are constituents of the adaptive immune response and accumulate within the plaques following lipid-specific activation by APCs. Recently it has been proposed that these two cell types can interact in a direct manner. However, no indication of such an interaction has been investigated in the context of
atherosclerosis
. In our study, we aimed to examine whether MCs can act as APCs in
atherosclerosis
, thereby modulating CD4
+
T cell responses. We observed that MCs increased their
MHC class II
expression under hyperlipidemic conditions both in vivo and in vitro. Furthermore, we showed that MCs can present Ags in vivo via
MHC class II
molecules. Serum from high-fat diet-fed mice also enhanced the expression of the costimulatory molecule CD86 on cultured MCs, whereas OVA peptide-loaded MCs increased OT-II CD4
+
T cell proliferation in vitro. The aortic CD4
+
and T
H1
cell content of atherosclerotic mice that lack MCs was reduced as compared with their wild-type counterparts. Importantly, we identified MCs that express HLA-DR in advanced human atheromata, indicating that these cells are capable of Ag presentation within human atherosclerotic plaques. Therefore, in this artice, we show that MCs may directly modulate adaptive immunity by acting as APCs in
atherosclerosis
.
...
PMID:Hypercholesterolemia Induces a Mast Cell-CD4
+
T Cell Interaction in Atherosclerosis. 3068 5
Depletion of B cells attenuates plaque development and modulates T cell responses in mouse models of
atherosclerosis
, suggesting that Ag presentation by B cells may promote disease progression. Thus, we set out to determine the role of B cell-mediated
MHC class II
(MHC II) Ag presentation during atherosclerotic plaque development. We developed murine conditional MHC II deletion and expression systems under control of the B cell-restricted CD19 promoter in an experimental model of
atherosclerosis
. Mice lacking MHC II expression only on B cells exhibited systemic shifts in germinal center and marginal zone B cell populations, leading to a reduced Ab response compared with littermate control animals. However, all populations were present and normal cholesterol uptake was detected in the plasma following high-fat diet treatment. In a second model, in which conditional expression of MHC II is limited only to B cells, showed similar overall cellularity characteristics compared with mice with complete MHC II deficiency. High-fat diet feeding showed no major changes in atherosclerotic plaque size or plaque cellular content in either conditional deletion or conditional expression approaches, compared with control animals. By testing the necessity and sufficiency of MHC II on B cells in the progression of
atherosclerosis
, we determine that MHC II on B cells does not directly regulate lesion development in murine models.
...
PMID:B Cell-Mediated Antigen Presentation through MHC Class II Is Dispensable for Atherosclerosis Progression. 3135 75
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