CD68 antigen expression by human retinal pigment epithelial cells

Elner, Susan G.; Elner, Victor M.; Nielsen, J C; Torczynski, Elise; Yu, Riley C.; Franklin, Wilbur A.

doi:10.1016/0014-4835(92)90087-9

Cited by 36 publications

(27 citation statements)

References 17 publications

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“…Although hum an RPE cells may express mono nuclear phagocyte CD68 antigen (Elner et al, 1992) we found no reactivity of rat RPE to monoclonal antibodies of the ED series. EAPU includes the migration of EDI + macrophages and T cells through the Bruch's membrane-RPE layer.…”

Section: Immune Mechanismcontrasting

confidence: 66%

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Macrophage Subpopulations and RPE Elimination in the Pathogenesis of Experimental Autoimmune Pigment Epithelial Protein-Induced Uveitis (EAPU)

Broekhuyse

Kuhlmann

Peters

et al. 1996

Experimental Eye Research

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Experimental autoimmune pigment epithelial protein-induced uveitis (EAPU) is a new type of disease that destroys the retinal pigment epithelium (RPE), and exhibits a hitherto unknown form of progressive chorioretinal dystrophy in which neuroretinal inflammatory foci are absent. The present study was aimed at studying the expression of adhesion molecules, and the kinetics of the appearance of the main types of macrophages and other intraocular immunocompetent cell populations in the various stages of this disease. EAPU was evoked in Lewis rats by immunization with the membrane protein from bovine RPE cells containing PEP-65 as main constituent, In the uvea, increased expression of intercellular adhesion molecule-1, of class II major histocompatibility complex antigen, and of ED2 macrophage reactivity were observed closely before the onset of EAPU. Expression of these reactivities was also slightly elevated by injections of the applied adjuvants alone. The onset of EAPU was mainly characterized by initial uveal infiltrations of EDI -I-macrophages and a minor population of CD4 T cells, and an increase in ED3, ED7 and perivascular ED2 reactive macrophages. This was followed by the development of focal accumulations of EDI + cells at both sides of the Bruch's membrane-RPE layer (Dalen-Fuchs nodules) which was permeated and disintegrated at these sites. The outer choroidal layer, the anterior iridal surface, and the base of the ciliary body more frequently contained active inflammatory cells than the other uveal areas. Lymphoid ceils were found scattered through the uvea, aqueous and vitreous. The sites of increased activity of ED2+ and ED3 + cells in the uvea were rather similar to those of EDI macrophages in the various stages of EAPU. Starting from multiple foci, the process of the formation of plaque-shaped cell accumulations in severe EAPU progressed along the RPE and exhibited a chronic character. The results of this study show that EDI +, ED2 +, ED3 + and ED7 -1-subpopulations of macrophages are actively involved in an immunopathological process in which the RPE is the target. The thickening of the plaque-shaped cell accumulations stops if the integrity of all RPE cells at that site has been affected. We postulate that this is the result of antigen elimination while additional influence of the abrogation of RPE cytokine production is presumed.

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Section: Immune Mechanismcontrasting

confidence: 66%

“…Pleiotropic cytokines like IL-1/? and GM-CSF (Planck et al, 1993), IL-6 (Benson et al, 1992), and MCP (monocyte chemotactic protein) (Elner et al, 1991) evade from the RPE cell layer after receiving a signal (e.g. IL-1, or TNF-a) from the activated immune system which attracts or stimulates immunocompetent cells.…”

Section: The Rpe In Eapumentioning

confidence: 99%

Macrophage Subpopulations and RPE Elimination in the Pathogenesis of Experimental Autoimmune Pigment Epithelial Protein-Induced Uveitis (EAPU)

Broekhuyse

Kuhlmann

Peters

et al. 1996

Experimental Eye Research

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“…In contrast to the pathologically transformed cells described above, these cells are involved in scavenging processes by phagocytosis of aged outer-segment membranes and share a panel of immunophenotypic antigen expression including HLA-DR, CD11c and CD14 with monocytes/macrophages. 29 The differentiation capacity of bone cells seems to have been underestimated in the past. Human bone-marrow fibroblasts have recently been shown to be able to differentiate into either adipocytes or osteogenic cells.…”

Section: Discussionmentioning

confidence: 99%

Human osteoblast-like cells phagocytose metal particles and express the macrophage marker CD68 in vitro

Heinemann

Lohmann²,

Siggelkow³

et al. 2000

The Journal of Bone and Joint Surgery. British volume

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P eriprosthetic osteolysis is a major cause of aseptic loosening in artificial joint replacement. It is assumed to occur in conjunction with the activation of macrophages. We have shown in vitro that human osteoblast-like cells, isolated from bone specimens obtained from patients undergoing hip replacement, phagocytose fine particles of titanium alloy (TiAlV).The human osteoblast-like cells were identified immunocytochemically by the presence of bone-specific alkaline phosphatase (BAP). With increasing duration of culture, a variable number of the osteoblastic cells became positive for the macrophage marker CD68, independent of the phagocytosis of particles, with a fine granular cytoplasmic staining which was coexpressed with BAP as revealed by immunodoublestaining. The metal particles were not toxic to the osteoblastic cells since even in culture for up to four weeks massively laden cells were vital and had a characteristic morphology. Cells of the human osteosarcoma cell line (HOS 58) were also able to phagocytose metal particles but had only a low expression of the CD68 antigen. Fluorescence-activated cell scanning confirmed our immunocytochemical results. Additionally, the cells were found to be negative for the major histocompatibility complex-II (MHC-II) which is a marker for macrophages and other antigen-presenting cells. Negative results of histochemical tests for tartrate-resistant acid phosphatase excluded the contamination by osteoclasts or macrophages in culture.Our observations suggest that the osteoblast can either change to a phagocytosing cell or that the phagocytosis is an underestimated property of the osteoblast. The detection of the CD68 antigen is insufficient to prove the monocytic lineage. In order to discriminate between macrophages and osteoblasts additional markers should be used. To our knowledge, this is the first demonstration of cells of an osteoblastic origin which have acquired a mixed phenotype of both osteoblasts and macrophages. Received 17 December 1998; Accepted after revision 21 May 1999Resorption of the surrounding bone is commonly associated with aseptic loosening of artificial joints.1-4 Particles of titanium, a common material used for endoprostheses, are released from the surfaces into the surrounding tissue by corrosion or wear. 3,4 The release of particulate wear debris is generally accepted to be responsible for the recruitment of monocytes/macrophages and the formation of foreign-body granulomas. Phagocytosis of wear particles by macrophages stimulates these cells to produce and secrete inflammatory mediators 5,6 which have been implicated in the stimulation of bone resorption. 7,8The role of osteoblasts in contact with wear particles is poorly understood. We have investigated the behaviour of cultured human osteoblast-like cells when exposed to metal particles in vitro. To exclude the presence of cells of myeloid origin, we also studied markers such as CD68, tartrate-resistant acid phosphatase (TRAP) and major histocompatibility complex II (MHC II). CD68 is used a...

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“…RPE cells possess macrophagelike properties, and have been shown to express hematopoietic cell markers in culture (Elner et al, 1992;Limb et al, 1997). Progressive retinal degeneration in Mitf vit/vit mutants is accompanied by a massive accumulation of 'macrophage-like' cells in the subretinal space between P21 and P60 (Boissy et al, 1987;Sidman et al, 1996), but it is not known if these cells are of monocyte-macrophage lineage, or alternatively, if they are RPE cells that have detached.…”

Section: Discussionmentioning

confidence: 99%

Altered expression of the iron transporter Nramp1 (Slc11a1) during fetal development of the retinal pigment epithelium in microphthalmia-associated transcription factor Mitfmi and Mitfvitiligo mouse mutants

Waes

Smith

Waes

et al. 2008

Experimental Eye Research

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Microphthalmia-associated Transcription Factor (Mitf) is expressed in neural crest cell-derived melanocytes, and in the retinal pigment epithelium (RPE) during ocular development. Mutations in Mitf are associated with auditory/visual/pigmentary syndromes in humans. Mitf mi/mi mouse mutants lack pigmentation, and are microphthalmic, while Mitf vit/vit mouse mutants display abnormal RPE pigmentation, and progressive retinal degeneration. Microarray analysis was used to identify novel downstream gene targets/pathways in the RPE that are altered by mutations in the transcription factor Mitf. Using the Affymetrix platform, gene expression profiles were generated using the eyes of E13.5 mouse fetuses that were wildtype, heterozygous, or homozygous for the Mitf mi mutation. In a separate experiment, eyes from E13.5 mouse fetuses homozygous for the Mitf vit mutation were compared to eyes from the C57BL/6 control background strain. Statistical analyses were performed using Robust Multiarray Average, mixed-effects ANOVA and random-variance t-tests. Altered expression of genes involved in pigment formation, melanosome biogenesis/transport, and redox homeostasis were observed. 12 genes were commonly mis-regulated in the eyes of both Mitf mutants: 10 of these genes were downregulated in both mutants relative to controls, while 2 of the genes (Nramp1 (Slc11a1) and epoxide hydrolase) were downregulated in Mitf mi/mi mutants, and conversely, upregulated in Mitf vit/vit mutants. Quantitative RT-PCR and immunohistochemistry were used to confirm altered gene/protein expression. RPE expression of the Fe +2 iron transporter Nramp1 (Slc11a1) has not previously been reported. Fe +2 is an important co-factor utilized by the iron-dependent isomerohydrolase RPE65 in the retinoid visual cycle. However, excess accumulation of Fe +2 in the RPE has recently been associated with oxidative damage and age-related macular degeneration. Abnormal pigmentation and increased activity of Slc11a1 in the RPE of Mitf vit mice may contribute to the pathology and progressive retinal degeneration observed in these mutants.

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CD68 antigen expression by human retinal pigment epithelial cells

Cited by 36 publications

References 17 publications

Macrophage Subpopulations and RPE Elimination in the Pathogenesis of Experimental Autoimmune Pigment Epithelial Protein-Induced Uveitis (EAPU)

Macrophage Subpopulations and RPE Elimination in the Pathogenesis of Experimental Autoimmune Pigment Epithelial Protein-Induced Uveitis (EAPU)

Human osteoblast-like cells phagocytose metal particles and express the macrophage marker CD68 in vitro

Altered expression of the iron transporter Nramp1 (Slc11a1) during fetal development of the retinal pigment epithelium in microphthalmia-associated transcription factor Mitfmi and Mitfvitiligo mouse mutants

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