Abstract：
:Much evidence indicates that atherosclerotic lesions are largely of an inflammatory nature. Activated macrophages and macrophage-derived foam cells laden with cholesterol esters are a major constituent of these lesions and can influence lesion formation via several potential mechanisms. One such mechanism is Fcgamma receptor activation and/or Fcgamma receptor-mediated clearance of immune complexes containing cholesterol, such as lipoprotein immune complexes. That this mechanism contributes to lesion formation would be further supported if Fcgamma receptor expression in arterial lesions were demonstrated. We therefore used monoclonal antibodies and immunocytochemical methods to analyze frozen sections of human arterial lesions for expression of each of the three primary classes of mononuclear phagocyte Fcgamma receptors. Approximately 800 sections of aorta, carotid, and coronary arteries obtained from five elderly donors were analyzed. The presence of macrophages was determined by assaying reactivity of a monoclonal antibody specific to CD163, which is expressed only on cells of the human mononuclear phagocyte lineage. Results indicate that highly cellular preatheromatous lesions contained numerous macrophages in the zone of proliferation that expressed each class of Fcgamma receptor (FcgammaRIA, FcgammaRIIA, and FcgammaRIIIA). Fcgamma receptor-positive cells were also present in medial and adventitial areas. Fcgamma receptor staining was both punctate and diffuse, the latter suggesting that soluble receptors were present in the extracellular matrix. These data further support that Fcgamma receptor-mediated clearance of immune complexes can occur in arterial lesions during atherogenesis. Expression of both the high affinity (FcgammaRIA) and lower affinity (FcgammaRIIA/FcgammaRIIIA) receptors indicates that mono- and multivalent IgG-containing immune complexes could engage Fcgamma receptors and influence lesion formation through several different inflammatory mechanisms triggered by receptor activation.
journal_name
Immunol Lettjournal_title
Immunology lettersauthors
Ratcliffe NR,Kennedy SM,Morganelli PMdoi
10.1016/s0165-2478(01)00217-6subject
Has Abstractpub_date
2001-07-02 00:00:00pages
169-74issue
3eissn
0165-2478issn
1879-0542pii
S0165247801002176journal_volume
77pub_type
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journal_title：Immunology letters
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journal_title：Immunology letters
pub_type： 杂志文章,评审
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更新日期：1999-03-01 00:00:00
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journal_title：Immunology letters
pub_type： 杂志文章,评审
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更新日期：2016-04-01 00:00:00
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journal_title：Immunology letters
pub_type： 杂志文章
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更新日期：2020-12-01 00:00:00
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journal_title：Immunology letters
pub_type： 杂志文章
doi：10.1016/j.imlet.2013.02.005
更新日期：2013-03-01 00:00:00
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pub_type： 杂志文章,评审
doi：10.1016/j.imlet.2007.04.013
更新日期：2007-07-31 00:00:00
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更新日期：1993-08-01 00:00:00
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journal_title：Immunology letters
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journal_title：Immunology letters
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abstract：:This article has been withdrawn at the request of the editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/our-business/policies/article-withdrawal. ...
journal_title：Immunology letters
pub_type： 撤回出版物
doi：10.1016/j.imlet.2017.08.015
更新日期：2017-08-26 00:00:00
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更新日期：1997-08-01 00:00:00
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journal_title：Immunology letters
pub_type： 杂志文章,评审
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journal_title：Immunology letters
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doi：10.1016/j.imlet.2020.04.005
更新日期：2020-07-01 00:00:00
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journal_title：Immunology letters
pub_type： 杂志文章
doi：10.1016/j.imlet.2016.06.005
更新日期：2016-09-01 00:00:00
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journal_title：Immunology letters
pub_type： 杂志文章
doi：10.1016/s0165-2478(99)00015-2
更新日期：1999-04-15 00:00:00
