Characterization and Expression of the Antigen Present on Resident Rat Macrophages Recognized by Monoclonal Antibody ED2

Barbé, Ellis; Damoiseaux, Jan; Döpp, E. A.; Dijkstra, Christine D.

doi:10.1016/s0171-2985(11)80586-3

Cited by 112 publications

(70 citation statements)

References 23 publications

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“…Approximately 30% of the CD45 ϩ cells in the cell suspensions of normal LEW hearts and isografts stained with the ED2 mAb, which has been reported to identify tissue macrophages 19,21 ( Fig. 2).…”

Section: Flow Cytometry Of Heart-cell Suspensionsmentioning

confidence: 86%

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Donor and recipient leukocytes in organ allografts of recipients with variable donor-specific tolerance: With particular reference to chronic rejection

et al. 2000

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We have attributed organ engraftment to clonal exhaustion-deletion of host-versus-graft and graft-versus-host reactions that are reciprocally induced and governed by migratory donor and recipient leukocytes. The so-called donor passenger leukocytes that migrate from the allograft into the recipients have been thoroughly studied (chimerism), but not the donor leukocytes that remain in, or return to, the transplanted organ. Therefore, using flow cytometry we determined the percentage and lineages of donor leukocytes in cell suspensions prepared from Lewis (LEW) cardiac allografts to 100 days posttransplantation. The LEW hearts were transplanted to naïve untreated Brown Norway (BN) recipients (group 2), to naïve BN recipients treated with a 28-day or continuous course of tacrolimus (TAC) (groups 3 and 4), and to drug-free BN recipients pretolerized by earlier bone marrow cell (BMC) or orthotopic LEW liver transplantation (groups 5 and 6). The findings in the heart cell suspensions were correlated with the results from parallel histopathologic-immunocytochemical studies and other studies of the grafts and of host tissues. Although the LEW heart allografts were rejected in 9.6 days by the unmodified recipients of group 2, all beat for 100 days in the recipients of groups 3 through 6. Nevertheless, all of the long-surviving cardiac allografts (but not the isografts in group 1) were the targets of an immune reaction at 5 days, reflected by dramatic increases in the ratio of leukocytes to nonleukocyte nucleated cells from normal values of 1:5-1:6 to 1:1-5:1 and by manifold other evidence of a major inflammatory event. The acute changes returned to baseline by 100 days in the chronic rejection (CR) free hearts of groups 4 and 6, but not in the CR-afflicted hearts of short-course TAC group 3 or the less-severely damaged hearts of the BMC-prime group 5.The freedom from CR in groups 4 and 6 was associated with a large donor contribution to the intracardiac leukocyte population at 5 days (28.6% and 22% in the respective groups) and at 100 days (30.5% in group 4 and 8.4% in group 6) compared with 2% and 1.2% at 100 days in the CR-blighted allografts of the partially tolerant animals of groups 3 and 5. Whether large or small, the donor leukocyte fraction always included a subset of class II leukocytes that had histopathologic features of dendritic cells. These class II ؉ cells were of mixed myeloid (CD11-b/c ؉ ) and lymphoid lineages; their migration was markedly inhibited by TAC and accelerated by donor-specific priming and TAC discontinuance. Although a large donor leukocyte population and a normal leukocyte/nonleukocyte cell ratio were associated with freedom from CR, these findings and the lineage profile of the intracardiac leukocytes were not associated with tolerance in the animals of groups 3 and 4 under active TAC treatment. The findings in this study, singly and in their entirety, are compatible with our previously proposed leukocyte migration-localization paradigm of organ allograft acceptance and tolerance. (Liver ...

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Section: Flow Cytometry Of Heart-cell Suspensionsmentioning

confidence: 86%

“…ED1 mAb was used to identify cells of the mononuclear/phagocyte system. 19,20 Tissue macrophages were identified with mAb ED2, 19,21 the specificity of which is similar to mAb BMAC-5. 22 …”

Section: Flow Cytometrymentioning

confidence: 91%

Donor and recipient leukocytes in organ allografts of recipients with variable donor-specific tolerance: With particular reference to chronic rejection

et al. 2000

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“…After two washes (10 min each), the sections were incubated for 48 h at 4°C with monoclonal antibodies against rat macro phages (mouse antirat ED2; Accurate Chemical and Sci entific Corporation, Westbury, NY, U.S.A.), which react with a membrane epitope in rat macrophages (Dijkstra et al, 1985;Barbe et al, 1990) and are expressed in the brain solely in the perivascular cells (Graeber et al, 1989). Thereafter, the sections were washed again three times (10 min each), and exposed to FITC-Iabeled goat antimouse antibodies (Jackson Laboratories) for 30 min at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Quantitation of Perivascular Monocytes and Macrophages around Cerebral Blood Vessels of Hypertensive and Aged Rats

Liu

Jacobowitz

Barone

et al. 1994

J Cereb Blood Flow Metab

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Summary: The numbers of monocytes and macrophages in the walls of cerebral blood vessels were counted on perfusion-fixed frozen brain sections (16 fLm) of sponta neously hypertensive rats (SHR), stroke-prone SHR (SHR-SP), normotensive Wistar-Kyoto (WKY) rats, and young (16-week-old) and old (2-year-old) normotensive Sprague-Dawley rats (SD-16w and SD-2y, respectively) using monoclonal antibodies against rat macrophages (ED2). The staining was visualized with fluorescein labeled second antibodies. The ED2-specific staining in brain sections was restricted to macrophages in a peri vascular location. The number of perivascular cells per square millimeter of high-power field was significantly greater in SHR-SP (8.6 ± 2.1; n = 4) and SHR (6.7 ± 0.9; n = 6) than in normotensive WKY (4.0 ± 0.5; n = 6; P

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“…3G-I, arrows). This immunoreactivity of minor intensity was attributed to Kupffer cells (liver macrophages), because in these areas, TGR5-immunoreactivity co-localized with ED2, a marker of macrophages 30 (Fig. 3J-L).…”

Section: Localization Of Tgr5 In Rat Livermentioning

confidence: 99%

The G-protein coupled bile salt receptor TGR5 is expressed in liver sinusoidal endothelial cells

et al. 2007

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Sinusoidal endothelial cells (SEC) constitute a permeable barrier between hepatocytes and blood. SEC are exposed to high concentrations of bile salts from the enterohepatic circulation. Whether SEC are responsive to bile salts is unknown. TGR5, a G-protein-coupled bile acid receptor, which triggers cAMP formation, has been discovered recently in macrophages. In this study, rat TGR5 was cloned and antibodies directed against the C-terminus of rat TGR5 were developed, which detected TGR5 as a glycoprotein in transfected HepG2-cells. B ile salts are required for cholesterol excretion and lipid absorption. 1 However, high concentrations of lipophilic bile salts have toxic effects. Bile salts alter membrane fluidity 2 and can act pro-or anti-apoptotic. [3][4][5][6] Many liver diseases are aggravated by the cholestatic potential of lipophilic bile salts. Therefore, several mechanisms exist to maintain bile salt homeostasis. These include the coordinated expression and action of bile salt transporters at the sinusoidal and canalicular membrane of liver parenchymal cells, 7 alternative pathways for bile salt synthesis and metabolism, 8,9 and the involvement of extrahepatic tissues (such as the gut and the kidneys) in bile salt excretion. [10][11][12] These mechanisms are closely regulated by nuclear receptors sensitive for bile salts, which control the expression of transporter proteins and enzymes. They comprise the farnesoid X receptor, 13-15 the pregnane X receptor, 16,17 and the vitamin D receptor. 18 Recently, a G-protein-coupled plasma membrane receptor responsive to bile salts has been discovered by highthroughput screening. This receptor, named TGR5, 19 M-BAR, or BG37, 20 stimulates adenylate cyclase on activation and increases the production of cyclic adenosine monophosphate (cAMP). Thereby, bile salts not only may be involved in the regulation of transcription but also may influence rapid, cAMP-dependent mechanisms in TGR5 expressing cells. So far, TGR5 expression has been demonstrated in enteroendocrine cells, 21 where bile salts stimulate the secretion of glucagon-like peptide-1 via TGR5 and in alveolar macrophages, 19 which secrete smaller amounts of cytokines in response to endotoxin, when bile salts are present. Recently, bile salts were shown to influence energy consumption in brown adipose tissue

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Characterization and Expression of the Antigen Present on Resident Rat Macrophages Recognized by Monoclonal Antibody ED2

Cited by 112 publications

References 23 publications

Donor and recipient leukocytes in organ allografts of recipients with variable donor-specific tolerance: With particular reference to chronic rejection

Donor and recipient leukocytes in organ allografts of recipients with variable donor-specific tolerance: With particular reference to chronic rejection

Quantitation of Perivascular Monocytes and Macrophages around Cerebral Blood Vessels of Hypertensive and Aged Rats

The G-protein coupled bile salt receptor TGR5 is expressed in liver sinusoidal endothelial cells

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