Membrane glycoprotein CD36: a review of its roles in adherence, signal transduction, and transfusion medicine

Greenwalt, Dale E.; Lipsky, RH; Ockenhouse, CF; Ikeda, Hisami; Tandon, NN; Ga, Jamieson

doi:10.1182/blood.v80.5.1105.bloodjournal8051105

Cited by 150 publications

(33 citation statements)

References 67 publications

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“…Starting with day 1, the 85 kD CD36 was scarcely visible in spite of a low platelet count (13 × 10 6 /ml), low haemoglobin (9 g/dl) and low haematocrit (28%). Since CD36 is found on a number of other cell membranes and tissues in addition to platelets (Greenwalt et al, 1992), it is possible that the anti-CD36 autoantibodies were reactive with many different cells and tissues, and not available in high concentration in the plasma. After 24 d the patient had a severe thrombotic crisis, and the platelet count dropped to 6 × 10 6 /ml, the haemoglobin to 6·7 g/dl, and the haematocrit to 19%.…”

Section: Characterization Of 85 Kd Cd36mentioning

confidence: 99%

“…The human CD36 is a single-chain integral membrane polypeptide (also known as GPIV; IIIb) expressed by platelets as well as many other cells, cell lines and tissues (Okumura & Jamieson, 1976;Asch et al, 1987;Tandon et al, 1989b;Greenwalt et al, 1990Greenwalt et al, , 1992. Numerous functions have been described for CD36, including a role as a cell surface receptor interactive with a large number of ligands, in cytoadhesion reactions, and implication in intracellular signal transduction (Jaffe et al, 1982;Leung, 1984;Silverstein et al, 1984Silverstein et al, , 1989Majack et al, 1988;Kieffer et al, 1989;Tandon et al, 1989a,b;Good et al, 1990;Murphy-Ullrich et al, 1992;Savill et al, 1992;Greenwalt et al, 1992;Endemann et al, 1993;Abumrad et al, 1993;Kehrel et al, 1998).…”

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Anti‐CD36 autoantibodies in thrombotic thrombocytopenic purpura and other thrombotic disorders: identification of an 85 kD form of CD36 as a target antigen

Schultz

Arnold

et al. 1998

Br J Haematol

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Summary. The presence of anti-CD36 antibodies in plasma of patients with thrombotic thrombocytopenic purpura (TTP), idiopathic thrombocytopenic purpura (ITP), and heparininduced thrombocytopenia without/with thrombosis (HIT/ HITT) has been examined by immunoblots, and a monoclonal antibody capture assay, the platelet-associated IgG characterization assay (PAICA). Results with PAICA showed that 73% (8/11) of patients with TTP were positive, and 71% (10/14) by immunoblots. With ITP, 20% (6/30) were positive by PAICA and 19% (3/16) by immunoblots; HIT, 30% (3/10) were positive by PAICA and 60% (6/10) by immunoblot; HITT, 50% (2/4) by PAICA and 100% (4/4) by immunoblot. Purification of CD36 by fast protein liquid chromatography (FPLC) from Triton X-100 extracts of normal platelet membranes resulted in the isolation of two different forms: the classic 88 kD form, and a second, lighter 85 kD form. Our data indicated that the patients' plasma autoantibodies reacted strongly with the 85 kD form. Conventional monoclonal and polyclonal antisera produced to the 88 kD form reacted strongly with the 88 kD form but weakly with the 85 kD form. These results confirm the possible importance of anti-CD36 antibodies in the pathophysiology of TTP and other thrombocytopenias and demonstrate the presence of a previously unrecognized target antigen for these antibodies.Keywords: thrombosis, thrombocytopenia, platelets, glycoform, immunoassays.The human CD36 is a single-chain integral membrane polypeptide (also known as GPIV; IIIb) expressed by platelets as well as many other cells, cell lines and tissues (Okumura & Jamieson, 1976;Asch et al, 1987;Tandon et al, 1989b;Greenwalt et al, 1990Greenwalt et al, , 1992. Numerous functions have been described for CD36, including a role as a cell surface receptor interactive with a large number of ligands, in cytoadhesion reactions, and implication in intracellular signal transduction (Jaffe et al, 1982;Leung, 1984;Silverstein et al, 1984Silverstein et al, , 1989Majack et al, 1988;Kieffer et al, 1989; Tandon et al, 1989a,b;Good et al, 1990;Murphy-Ullrich et al, 1992;Savill et al, 1992;Greenwalt et al, 1992;Endemann et al, 1993;Abumrad et al, 1993;Kehrel et al, 1998).The molecular mass of CD36 on different cells is variable; for example, M r values of 88 000, 85 000 and 78 000 have been reported for human platelets, human mammary epithelial cells, and human erythroblasts, respectively (Tandon et al, 1989b;Greenwalt et al, 1990;Kieffer et al, 1989).A cDNA clone encoding CD36 was isolated from a human placenta cDNA library and expressed in COS cells by Oquendo et al (1989), resulting in a polypeptide with 471 residues and a predicted M r of approximately 53 kD. The identification of 10 potential N-linked glycosylation sites accounted for the difference in M r between the polypeptide and the 83 kD species found by immunoprecipitation with a pool of mouse monoclonal anti-CD36 antibodies. Tandon et al (1989b) purified CD36 from solubilized Triton X-114 extracts of human platelet membranes, and report...

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Section: Characterization Of 85 Kd Cd36mentioning

confidence: 99%

mentioning

confidence: 99%

Anti‐CD36 autoantibodies in thrombotic thrombocytopenic purpura and other thrombotic disorders: identification of an 85 kD form of CD36 as a target antigen

Schultz

Arnold

et al. 1998

Br J Haematol

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“…Recently, Schultz et al (1998) reported that the plasmas of 8/11 patients with TTP were reactive to CD36, and provided evidence that patient antibodies preferentially recognize a 85 kD form of CD36. CD36 occurs in platelets and endothelial cells, as well as in other cells and tissues (Greenwalt et al, 1992). Given the predilection of microvascular involvement in TTP, and the anatomic restriction of CD36 expression in microvascular endothelial cells, but not on endothelial cells of large vessels (Swerlick et al, 1992), we investigated reactivity of sera from patients with TTP against large and small vessel endothelial cells before and after plasma exchange therapy.…”

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confidence: 99%

Characterization of platelet glycoproteins and platelet/endothelial cell antibodies in patients with thrombotic thrombocytopenic purpura

et al. 1999

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Platelets and sera from 12 patients with thrombotic thrombocytopenic purpura (TTP) and 12 healthy normal control subjects were examined. As determined by quantitative flow cytometry, prior to plasma exchange therapy platelet surface glycoprotein (GP) Ib levels were similar in TTP patients and normal controls (mean 20 188 and 20 226 molecules/platelet, respectively). Platelets from patients with TTP did, however, have significantly reduced levels of GPIIb/IIIa prior to plasmapheresis (mean 36 348 v 52 505 molecules/platelet in controls; P = 0.0004) and of GPIV (mean 13 321 v 26 212 molecules/platelet in controls; P = 0.0002). An increase in activated platelets, as determined by CD62 expression, was observed in 82% of patients. Increased platelet-associated immunoglobulins and/or complement was also seen in approximately 60% of the patients. In general, with return of platelet counts to normal levels following seven plasmaphereses, the above abnormalities were reversed, although often not to normal levels. Western blot analysis indicated the presence of antibodies reactive to platelet GPIV (88 kD) in 70% of pretreatment sera from patients with TTP; a similar band was observed in 80% of patient sera against microvascular endothelial cells. Immunofluorescence microscopic examination indicated the presence of antibody in pretreatment sera from patients with TTP to microvascular (73%) and large vessel (36%) endothelial cells. As measured by an indirect flow cytometric assay, pretreatment sera from 55% of patients with TTP were reactive with large vessel endothelial cells and 100% reacted with microvascular endothelial cells; reactivity was significantly greater against the microvascular endothelial cells (P = 0.0048) and was reduced following plasma exchange therapy. These results indicate abnormalities in platelet glycoprotein expression in TTP and suggest that anti-platelet and anti-endothelial cell antibodies play a role in the thrombocytopenia and vasculitis characteristic of this disorder.

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“…Class A and class B can be further divided into many types, including SR‐AI, SR‐AII, SR‐AIII, SR‐BI, SR‐BII and SRBIII [27,37]. SRBIII, also termed CD36, is mainly expressed on cells of lymphoid and hematopoietic lineages, such as monocytes, Mø, platelets, endothelial cells and a variety of cultured cell lines [38,39]. MR is a carbohydrate‐binding receptor mainly expressed by Mø and DCs [30].…”

Section: Discussionmentioning

confidence: 99%

Leukocyte immunoglobulin-like receptor A3 is increased in IBD patients and functions as an anti-inflammatory modulator

Lan

Liu

et al. 2020

Clinical and Experimental Immunology

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Summary Growing evidence shows that a homozygous 6·7-kb deletion of the novel anti-inflammatory molecule leukocyte immunoglobulin-like receptor A3 (LILRA3) is associated with many autoimmune disorders. However, its effects on pathogenesis of inflammatory bowel disease (IBD) have yet not been clarified. LILRA3 is mainly expressed in monocytes, whereas its effects on biological behaviors of monocytes have not been systematically reported. In our study, to investigate the association between LILRA3 polymorphism and IBD susceptibility, LILRA3 polymorphism was assessed in 378 IBD patients and 509 healthy controls. Quantitative real time PCR (qRT–PCR), Western blot and immunohistochemistry (IHC) were employed to detect the LILRA3 expression in IBD patient blood and intestinal samples. The human U937 monocyte cell line was employed to establish LILRA3 over-expressing cells and the effects of LILRA3 on the biological behaviors of U937 cells were systematically explored. Although no association of the polymorphism with IBD development was found, LILRA3 expression was markedly increased in IBD patients compared with healthy controls. Over-expression of LILRA3 in monocytes led to significant decreases in secretion of interferon (IFN)-γ, tumor necrosis factor (TNF)-α and interleukin (IL)-6. Additionally, LILRA3 abated monocyte migration by reducing the expression of several chemokines and enhanced monocyte phagocytosis by increasing CD36 expression. Furthermore, LILRA3 promoted monocyte proliferation through a combination of Akt and extracellular receptor kinase/mitogen-activated protein kinase (Erk/MEK) signaling pathways. We report for the first time, to our knowledge, that LILRA3 is related to IBD and functions as an anti-inflammatory modulator in U937 cells.

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Membrane glycoprotein CD36: a review of its roles in adherence, signal transduction, and transfusion medicine

Cited by 150 publications

References 67 publications

Anti‐CD36 autoantibodies in thrombotic thrombocytopenic purpura and other thrombotic disorders: identification of an 85 kD form of CD36 as a target antigen

Anti‐CD36 autoantibodies in thrombotic thrombocytopenic purpura and other thrombotic disorders: identification of an 85 kD form of CD36 as a target antigen

Characterization of platelet glycoproteins and platelet/endothelial cell antibodies in patients with thrombotic thrombocytopenic purpura

Leukocyte immunoglobulin-like receptor A3 is increased in IBD patients and functions as an anti-inflammatory modulator

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