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At least 19 recordsLinked to original sources
PubMed1992

Epitopic heterogeneity of the CD36 antigen expressed by normal and neoplastic endothelial cells. An immunohistochemical study with a novel monoclonal antibody 8C9.

Phenotypic and functional heterogeneity of endothelial cells (ECs) is being recognized with increasing frequency. Here we report a novel murine monoclonal antibody (MoAb), named 8C9, that detects a unique epitope on the leukocyte differentiation antigen CD36 (platelet glycoprotein IV or IIIb) expressed by both normal and neoplastic ECs. In immunohistochemical and flow-cytometric studies, 8C9-immunoreactivity was detected on capillary ECs, adipocytes, monocytes, platelets and a human monocytoid cell line U-937, which are known to express the CD36 antigen. Blocking experiments using U-937 cells and studies on cryostat sections revealed that a murine MoAb OKM5, which detects the CD36 antigen, blocked the binding of 8C9 to its antigen. Immunoblot analysis showed that 8C9 bound to a 97-kDa membrane protein expressed by U-937 cells treated with phorbol ester. These results indicate that 8C9 detects the CD36 antigen. However, the findings that some OKM5-positive normal ECs in the liver, spleen and lymph nodes as well as neoplastic ECs in a cutaneous angiosarcoma did not react with 8C9, together with the fact that the CD36 antigen does not form a complex or associate with other proteins, suggest epitopic heterogeneity of the CD36 antigen expressed by these tissues.

Antibodies, Monoclonal↗
PubMed1991

Keratinocyte expression of CD36 antigen in benign and malignant epidermal cell-derived tumours.

Keratinocytes express the macrophage/monocyte antigen CD36 in a variety of inflammatory cutaneous diseases characterised by a T lymphocyte rich infiltrate. Since cell-mediated immune mechanisms also play a role in host responses to skin tumours, we investigated the presence of CD36 antigen on keratinocytes in a range of epidermal cell-derived benign and malignant tumours characterised by a peritumoural, dermal lymphocytic infiltrate. Frozen tissue sections of lesional tissue from a range of epidermally derived tumours were labelled with antibodies to CD1a, CD11b, CD36, and HLA-DR antigens. Benign and malignant squamoproliferative tumour cells exhibited a spectrum of CD36 expression, whereas those of basal cell origin were consistently CD36-. Suprabasal expression of CD36 was present in the normal perilesional epidermis of all tumours studied including basal cell carcinoma. Keratinocyte CD11b expression was not observed. The widespread presence of keratinocyte CD36 positivity in squamoproliferative, but not basal epidermal, tumours suggests its expression may be linked to the degree of keratinocyte differentiation. The stimulus for expression is unknown, but the fact that suprabasal perilesional epidermis expressed CD36 strongly in the absence of infiltrate suggests it may represent a non-specific response by keratinocytes to various stimuli.

Adult↗
PubMed1995

Identification of an immunodominant functional domain on human CD36 antigen using human-mouse chimaeric proteins and homologue-replacement mutagenesis.

The human CD36 antigen is a multifunctional membrane glycoprotein that acts as a receptor for thrombospondin, malaria-infected erythrocytes and oxidized low-density lipoprotein, as well as being implicated in the recognition of apoptotic neutrophils by macrophages. OKM5 and other anti-CD36 monoclonal antibodies have been shown to inhibit these CD36 adhesive functions, suggesting that the monoclonal-antibody epitopes and the domains that mediate these events are closely related. Analysis of a series of chimaeric exchanges between human and mouse CD36 shows that six anti-CD36 monoclonal antibodies (OKM5, FA6-152, L103, 5F1, SM phi and 10/5) recognize epitopes within the domain comprising amino acids 155-183. A seventh monoclonal antibody (13/10) binds to another domain that spans amino acids 30-76. Homologue-replacement mutagenesis performed within the human 155-183 immunodominant sequence identifies key residues for the binding of three functional monoclonal antibodies (OKM5, FA6-152 and L103). The fact that antibodies directed against the 155-183 domain can inhibit adhesion suggests that this domain is directly involved in CD36-ligand binding.

Amino Acid Sequence↗
PubMed1990

Knob-independent cytoadherence of Plasmodium falciparum to the leukocyte differentiation antigen CD36.

The survival of Plasmodium falciparum-infected erythrocytes is enhanced by the sequestration of mature trophozoites and schizonts from the peripheral circulation. Cytoadherence of infected erythrocytes in vivo is associated with the presence of knobs on the erythrocyte surface, but we and others have shown recently that cytoadherence to C32 melanoma cells may occur in vitro in the absence of knobs. We show here that a knobless clone of P. falciparum adheres to the leukocyte differentiation antigen, CD36, suggesting that binding to CD36 is independent of the presence of knobs on the surface of the infected erythrocyte. This clone showed little cytoadherence to immobilized thrombospondin or to endothelial cells expressing the intercellular adhesion molecule 1. Furthermore, an Mr approximately 300-kD trypsin-sensitive protein doublet was immunoprecipitated from knobless trophozoite-infected erythrocytes. Finding a P. falciparum erythrocyte membrane protein 1 (PfEMP1)-like molecule on these infected erythrocytes is consistent with a role for PfEMP1 in cytoadherence to CD36 and C32 melanoma cells.

Animals↗
PubMed1990

Different expression of CD36 antigen molecule on the surface of megakaryocyte lineage leukemias and megakaryocyte leukemia cell lines MEG-01 and HEL.

Peripheral blood leukemic cells from four patients with peroxidase negative acute leukemia, which expressed neither myeloid nor lymphoid cell surface antigens, were analyzed by using monoclonal antibodies (MoAb) capable of recognizing megakaryocyte-platelet-related antigens. Leukemic cells from one case reacted with 5F1 MoAb, whereas cells from all the tested cases reacted with OKM5 MoAb, which belongs to the same CD group as 5F1 (CD36). Also, culture cells from megakaryoblastic leukemia cell line, MEG-01, and human erythroleukemia cell line, HEL, showed a different pattern of expression for the CD36 antigen molecule detected by 5F1 and OKM5 MoAb, individually. Furthermore, we have demonstrated that the epitopes recognized by 5F1 and OKM5 MoAb appear on the same CD36 molecule on the surface of HEL cells by means of the two-color analysis using FACS-IV. On the basis of our experiments, we conclude that, CD36 molecule, a receptor for TSP, is synthesized and expressed in at least two ways, inside the cells and on the surface of megakaryocyte lineage leukemias and megakaryocytic leukemia cell lines MEG-01 and HEL. This is strongly suggestive that thrombospondin (TSP)-mediated adhesion represents an alternative pathway for cytoadherence, and that CD36 expression on various kinds of cells may lack some essential modifications or components necessary for the TSP receptor activity.

Antibodies, Monoclonal↗
PubMed1994

[Expression of the OKM5 antigen (CD36) in normal keratinocytes and inflamed mucosa].

In 62 oral mucosa biopsies of different localization and diagnoses, immunohistochemically investigated with the APAAP technique, the OKM5 expression on keratinocytes was connected with the epithelial keratinization. In parakeratotic epithelia, an obvious CD36 upregulation was detectable. Surprisingly, there was no correlation between neither the state of inflammation nor the diagnoses and the OKM5 keratinocyte expression; the oral localization by itself appeared to be responsible for the CD36 expression.

Adolescent↗
PubMed1994

Expression of the myelomonocytic antigens CD36 and L1 by keratinocytes in squamous intraepithelial lesions of the cervix.

The keratinocytes in squamous intraepithelial lesions (SILs) of the cervix show altered expression of a number of molecules involved both in the control of growth and differentiation and in cell surface interactions, particularly with components of the immune system. We have used tissue biopsies and in vitro model systems to investigate the expression in SILs of the molecules CD36 and L1, which are predominantly expressed by myelomonocytic cells but which also have functional roles in keratinocyte biology. Whereas the L1 protein (defined by the monoclonal antibody Mac387) was expressed by suprabasal and superficial cells in 12 of 12 cases of normal cervix (NCx) and in 14 of 14 cases of low-grade SILs (LG-SILs), in two of 16 cases of high-grade SILs (HG-SILs) it was entirely absent and in the remainder it was restricted to the most superficial layers. When an arbitrary grading scale was applied, L1 expression in HG-SILs proved to be significantly lower than in LG-SILs (P < .01) or in cases of NCx (P < .01). CD36 was expressed by superficial cells in four of 12 cases of NCx, in six of 14 LG-SILs, and none of 16 cases of HG-SILs (when graded, LG-SILs v HG-SILs = P < .05). The mechanisms underlying the expression of both molecules were investigated by growth in organotypic tissue culture of normal ectocervical epithelium and the cervical keratinocyte cell lines W12 (a model for LG-SILs) and CaSki and SiHa (models for HG-SILs). L1 was diffusely expressed by NCx cells and the W12 cell line, although its expression in the CaSki and SiHa cell lines was much more irregular and restricted. CD36 was occasionally present on the surface of superficial NCx and W12 cells, but was absent from CaSki and SiHa cells. Neither molecule could be induced by treatment of the cells with interferon-gamma. These data suggest that the expression of CD36 and L1 by cervical keratinocytes is related to their differentiation status rather than representing an effect of exogenous factors, such as those released by the immune cell infiltrate associated with SILs. CD36 may function as an immunoregulatory molecule on cervical keratinocytes in SILs, while L1 is more likely to be involved in the intracellular regulation of cell proliferation and maturation.

Antigens, CD↗
PubMed1994

Src-related protein tyrosine kinases are physically associated with the surface antigen CD36 in human dermal microvascular endothelial cells.

Src-related cytoplasmic PTKs are physically and functionally associated with cell surface receptors and are involved in signal transduction. In this paper we report the identification of src-related proteins p59fyn, pp60c-src and p62yes in human microvascular endothelial cells cultured from normal human skin and their physical association with the thrombospondin receptor CD36. Such an association represents a potential signalling pathway by which thrombospondin may regulate angiogenesis.

Antigens, CD↗
PubMed1994

Mast cell growth factor modulates CD36 antigen expression on erythroid progenitors from human bone marrow and peripheral blood associated with ongoing differentiation.

To study the differentiation process of erythroid progenitors from normal human bone marrow and peripheral blood, CD34/CD36 sorted cells were cultured in the presence of Erythropoietin (Epo) and Epo plus mast cell growth factor (MGF). The CD34+/CD36- cell fraction from bone marrow supported 74 +/- 33 erythroid burst forming units (BFU-E)/10(4) cells (mean +/- SD, n = 4) in the presence of Epo, which increased 2.1-fold by coculturing with MGF. However, erythroid colony-forming units (CFU-E) were not cultured from the CD34+/CD36- cell fraction. In contrast, the CD34-/CD36+ cell fraction supported CFU-Es in the presence of Epo (152 +/- 115/10(5)) or Epo plus MGF (180 +/- 112/10(5)), whereas BFU-Es were hardly noticed. However, the transition of the BFu-E to CFU-E was observed by incubating CD34+/CD36- cells (10(4)/100 microL) in suspension with Epo plus MGF for 7 days followed by Epo in the colony assay. This was reflected by the appearance of CD34-/CD36+/Glycophorin A+/CD14- cells. In addition high numbers of CFU-Es (1,000 +/- 150, n = 4) were cultured from this cell fraction. In contrast to bone marrow erythroid progenitors, no peripheral blood CFU-Es were cultured from either the CD36+ or CD36- fraction, whereas BFU-Es were predominantly present in the CD36+ fraction. However, the CD34+ progenitor cell from peripheral blood did have intrinsic capacity to differentiate to CFU-Es because CD34+/CD36- cells incubated with Epo plus MGF for 7 days and followed by Epo in the colony assay, supported high numbers of CFU-Es (1,200 +/- 400, n = 3). To study whether additional growth factors have similar effects on erythroid progenitors, experiments were performed with interleukin 1 (IL-1), IL-3, and IL-6. IL-1 and IL-6 did not modulate the Epo supported proliferation and differentiation. In contrast, IL-3 in the presence of Epo did support CFU-Es, from CD34+/CD36- cells after 7 days in suspension culture. However, flow cytometry analysis showed that Epo plus IL-3 not only supported CD34-/CD36+/Glycophorin A+ cells but also CD36+/CD14+ cells, indicating the differentiation along different cell lineages. In summary, the data show a phenotypic distinction between bone marrow and peripheral blood erythroid progenitors with regard to CD36 expression. In addition, the results suggest that Epo plus MGF or IL-3 and preincubation in suspension culture are prerequisites for the transition of the BFU-E to the CFU-E.

Antigens, CD↗
PubMed1989

Expression of CD36 (OKM5) antigen on epidermal cells in normal and diseased skin.

The expression of the CD36 (OKM5) antigen was studied with the PAP technique on sections of skin from healthy subjects and of normal and diseased skin from patients with various skin diseases. In specimens from healthy subjects the antigen was found on vascular and perivascular structures and in some cases it was seen on cells of the acrosyringium. A net-like pattern of CD36 was observed in the upper part of the stratum spinosum in skin lesions of patients with psoriasis, lichen planus, pityriasis rosea, morbilliform drug reactions, necrobiosis lipoidica, lichen amyloidosus, Darier's disease and ichthyosis vulgaris. Expression of CD36 was also seen in the nonlesional skin just below the granular layer in 3 of 5 patients with factitial urticaria with immediate dermographism, but not in delayed dermographism or chronic urticaria. In ichthyosis vulgaris CD36 was also expressed in dendritic cells of the basal layer and in a patient with a graft versus host reaction it was recognized both on scattered keratinocytes and on dendritic cells in the epidermis. The role of the expression of the CD36 antigen in the skin is unknown. The activated cells might possibly serve as antigen-presenting cells and/or have a modulatory influence on an inflammatory reaction.

Antibodies, Monoclonal↗
PubMed1994

Cell surface antigen expression in human erythroid progenitors: erythroid and megakaryocytic markers.

This review summarizes the changes in cell surface antigen expression during proliferation and differentiation of human erythroid progenitors. The content is based on our experimental data obtained from complement-mediated cytotoxicity assays against hematopoietic progenitors and a combined technique of sequential micromanipulations of paired daughter cells derived from erythroid burst-forming units (BFU-E) and immunostaining with a panel of monoclonal antibodies, as well as from current information. BFU-E has CD34, CD41a (platelet glycoprotein[GP]IIb/IIIa) and CD41b(GPIIb) antigens. Paired daughter cells derived from BFU-E have CD41a, CD41b, CD71 (transferrin receptor) and HLA-DR antigens, but not CD34 or CD33 antigen. The CD36 antigen (thrombospondin receptor or GPIV) is first expressed on the cells after 5 days of culture, in agreement with the report that the anti-CD36 positive fraction contained a greater part of the erythroid colony-forming units (CFU-E). The blood group A antigen is first expressed on cells from aggregates derived from BFU-E after 5 days of culture. Glycophorin A is expressed on cell surface after 7 days of culture when proerythroblasts first appear. Hemoglobin alpha is expressed after 8 days of culture and coincides with the first appearance of basophilic erythroblasts. This review provides useful information on the identification of leukemic cells from poorly differentiated acute leukemias such as early erythroblastic leukemia and acute megakaryoblastic leukemia, and is useful in the understanding of the commitment and differentiation of erythroid and megakaryocytic progenitors in normal hematopoiesis.

Antigens, Surface↗
PubMed2007

The gamma-globin gene promoter progressively demethylates as the hematopoietic stem progenitor cells differentiate along the erythroid lineage in baboon fetal liver and adult bone marrow.

OBJECTIVE: To determine whether the difference in gamma-globin gene promoter methylation in terminal erythroblasts at the fetal and adult stages of development is a result of fetal stage-specific demethylation or adult stage-specific de novo methylation during erythropoiesis. MATERIALS AND METHODS: Fetal liver- (FL, n = 2) and adult bone marrow- (ABM, n = 3) derived hematopoietic stem/progenitor cells and mature erythroblasts were purified by passage through a Miltenyi Magnetic Column followed by fluorescein-activated cell sorting (FACS) into subpopulations, defined by expression of CD34 and CD36 antigens. CD34(+)CD36(-), CD34(+)CD36(+), and CD34(-)CD36(+) subpopulations were purified by FACS and their degree of differentiation verified using the colony-forming cell assay. The methylation pattern of 5 CpG sites in the gamma-globin promoter region of these purified cell populations was determined using bisulfite sequencing. RESULTS: The gamma-globin promoter was highly methylated in the earliest stage of hematopoietic stem progenitor cells (CD34(+)CD36(-)) and methylation progressively decreased as erythroid differentiation progressed in FL and appears so in ABM as well. CONCLUSIONS: These data support a model in which differences in the methylation pattern of the gamma-globin gene in differentiating erythroblasts at different stages of development is the result of fetal stage-specific demethylation associated with transcriptional activation, rather than de novo methylation in the adults. The difference in the extent of gamma-globin gene demethylation in FL and ABM is correlated with the difference in gamma-globin expression at these developmental stages.

Animals↗
PubMed1997

CD36 (OKM5) antigen expression on human mucosal epithelia is associated with keratinization type.

The glycoprotein CD36 functions as a thrombospondin receptor and is expressed on a variety of cell types, including platelets, monocyte/macrophages, and endothelial cells. In human skin, the presence of CD36 on keratinocytes was initially found in lesional areas of T-cell mediated inflammatory dermatoses. Controversy still exists on the interpretation of this expression as an inflammatory or differentiation-associated marker. So far, only limited data are available on CD36 expression in oral epithelia. The present immunohistochemical study was therefore performed to determine the presence of CD36 on keratinocytes of healthy and disease-affected epithelia of the oral cavity in 80 biopsy specimens. As results, we found an inflammation-independent strong expression of CD36 in oral epithelia with ortho- and parakeratinization, such as the oral side of the gingiva, the hard palate, and the back of the tongue. Non-keratinized epithelia such as the gingival pocket epithelium, the soft palate, the lip, the buccal mucosa, and the side of the tongue were CD36 negative. We therefore suggest that CD36 expression in keratinocytes from oral epithelia is an epithelial differentiation marker.

Adolescent↗
PubMed1995

Mechanisms of cytoadhesion of flowing, parasitized red blood cells from Gambian children with falciparum malaria.

Adhesion of parasitized red blood cells to vascular endothelium is considered to be a major factor in the pathophysiology of falciparum malaria, and so the molecular mechanisms and rheologic characteristics of this interaction are of profound importance. We have investigated the adhesive behavior of wild-type parasite isolates cultured from the blood of Gambian children with falciparum malaria and allowed to flow over surfaces coated with formaldehyde-fixed human umbilical vein endothelial cells (HUVEC) or platelets. Parasitized cells were able to attach to HUVEC and/or to platelets, and studies with monoclonal antibodies showed that intercellular adhesion molecule-1 (ICAM-1) and CD36 antigen were the major mediators of adhesion for the two surfaces, respectively. The levels of adhesion to HUVEC and to platelets were highly variable but did not correlate with each other, so that different isolates express independently variable capacities to bind to the two receptors. Adhesion was stationary for platelets and generally at a higher level compared with binding to HUVEC, which was predominantly (about 60%) of a rolling type. The stationary component of adhesion to HUVEC represented a greater proportion of adhesion for the wild isolates than for laboratory-adapted strains, and this form of adhesion was relatively insensitive to antibody to ICAM-1. This suggests the existence of an additional endothelial cell-expressed receptor for the wild isolates. These studies show wide variation in the ability of wild isolates of Plasmodium falciparum to adhere to ICAM-1, CD36 antigen, and possibly other receptors in the presence of physiologically relevant flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Identification of endothelial antigens relevant to transplant coronary artery disease from a human endothelial cell cDNA expression library.

Accelerated transplant coronary artery disease (TxCAD) results in increased expression of antiendothelial antibodies whose target antigens remain largely unidentified. One of these endothelial antigens has been identified as vimentin, a cytoskeletal protein present in cells of the blood vessel walls. In the present study, SDS-PAGE and Western blot analysis of human endothelial cell (EAHy 926) lysates probed with sera from a TxCAD patient were used to confirm immunoreactivity of antiendothelial antibodies towards several endothelial proteins. To further elucidate the identity of these putative antigens, a human endothelial cell (EAHy 926) cDNA expression library was immunoscreened with serum obtained from a TxCAD patient. Two positive cDNA clones were identified by partial nucleotide sequence analysis and GenBank/EMBL database searches for homology as the 85 kDa human CD36 antigen (a cell surface glycoprotein expressed in various cells including epithelial and endothelial cells) and a 50 kDa keratin-like protein (a member of the intermediate filament protein expressed in epithelial cells). These results are the first to demonstrate that human CD36 antigen and a keratin-like protein may be additional target proteins for the anti-endothelial antibodies associated with TxCAD.

Antibodies↗
PubMedDate not supplied

Histiocytes in familial and infection-induced/idiopathic hemophagocytic syndromes may exhibit phenotypic differences.

Familial hemophagocytic syndrome (FHS) and infection-associated hemophagocytic syndrome (IAHS) usually present with fever, pancytopenia, hepatosplenomegaly, signs of hepatic dysfunction, bleeding diathesis, and neurological manifestations. FHS is almost uniformly fatal, and IAHS is associated with high mortality. The only distinguishing characteristics are lack of family history and association with infection in the latter. Despite this, sporadic cases of FHS and culture-negative examples of IAHS (idiopathic HS) can be difficult to distinguish and the distinction may have important implications for treatment and family planning. We evaluated the immunophenotype of the macrophages (M phi s) in frozen tissue sections from three cases of hemophagocytic syndrome using a very large panel of monocyte/M phi-associated monoclonal antibodies and an immunoperoxidase technique. The clinical and laboratory features suggested that two were examples of FHS (one with strong family history) and that the third was IAHS/idiopathic HS. The results supported the clinical impressions by showing that the antigenic phenotypes of the FHS cases were nearly identical and different from that of the case of presumed IAHS/idiopathic HS. Specifically, M phi s from the FHS cases expressed complement receptors, 1, 2, and 3 (CD35, CD21, and CD11b, respectively), the monocyte antigen CD36, and the "activation" antigens CD25 (IL2-R) and CD30 (Ki-1), while those from the IAHS/idiopathic case did not. These studies also demonstrated that the M phi s in these cases exhibited some phenotypic differences from those in control tissues, that is, expression of the pan-M phi antigen CD14, the M phi subset antigen identified by antibody G16/1, complement receptors, certain monocyte antigens, and M phi "activation" antigens.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗