Disregulation of leukosialin (CD43, Ly48, sialophorin) expression in the B-cell lineage of transgenic mice increases splenic B-cell number and survival.

Dragone, Leonard L.; Barth, Richard K.; Sitar, Kristie L.; Disbrow, Gary L.; Frelinger, John G.

doi:10.1073/pnas.92.2.626

Cited by 54 publications

(26 citation statements)

References 53 publications

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“…In the B-cell lineage, CD43 is present on the cell surface of terminally differentiated cells causing prolonged survival, but not in less-differentiated cells (Dragone et al, 1995;Rosenstein et al, 1999). The reason for CD43 not being studied in other cell types is that CD43 has long been considered as an exclusive leukocyte marker.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of leukocyte marker CD43 causes activation of the tumor suppressor proteins p53 and ARF

2003

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CD43 or leukosialin is a transmembrane sialoglycoprotein, whose extracellular domain participates in cell adhesiveness and the cytoplasmic tail regulates a variety of intracellular signal transduction pathways involved in cell proliferation. CD43 is abundantly expressed on the surface of hematopoietic cells, but CD43 expression is also frequently found in the tumor cells of nonhematopoietic origin. In the early stages of some tumors, the accumulation of tumor suppressor protein p53 has been described. Here, we show that the expression of CD43 causes the induction of functionally active p53 protein.Moreover, we found that the activation of p53 by CD43 is mediated by tumor suppressor protein ARF. The coexpression of CD43 and ARF in ARF-null mouse embryonic fibroblasts resulted in programmed cell death, but that was not the case when CD43 alone was expressed in these cells. These data provide the first evidence of the connection between p53-and CD43-dependent pathways.

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Section: Introductionmentioning

confidence: 99%

Overexpression of leukocyte marker CD43 causes activation of the tumor suppressor proteins p53 and ARF

2003

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“…Involvement of CD43 in leukocyte homing and tissue infiltration, possibly due to its adhesive or anti-adhesive properties, has been shown in several studies (19,25,26). It has also been demonstrated that CD43 can regulate cell survival (27,28) and is involved in the apoptosis of T cells and hemopoietic progenitor cells (29 -32).…”

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confidence: 99%

CD43 Is Required for Optimal Growth Inhibition of Mycobacterium tuberculosis in Macrophages and in Mice

Randhawa

Ziltener

Merzaban

et al. 2005

The Journal of Immunology

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We explored the role of macrophage (Mφ) CD43, a transmembrane glycoprotein, in the pathogenesis of Mycobacterium tuberculosis. Using gene-deleted mice (CD43−/−), we assessed the association of the bacterium with distinct populations of Mφ and found that CD43−/− Mφ bound less M. tuberculosis than CD43+/+ Mφ. Increased infective doses did not abrogate this difference. However, reduced association due to the absence of CD43 could be overcome by serum components. Mφ from heterozygote mice, which express 50% of wild-type CD43, bound more bacteria than CD43−/− but less than CD43+/+, proving that the gene dose of CD43 correlates with binding of M. tuberculosis. Furthermore, the reduced ability of CD43−/− Mφ to bind bacteria was restricted to mycobacterial species. We also found that the survival and replication of M. tuberculosis within Mφ was enhanced significantly in the absence of CD43, making this the first demonstration that the mechanism of mycobacterial entry influences its subsequent growth. Most importantly, we show here that the absence of CD43 in mice aerogenically infected with M. tuberculosis results in an increased bacterial load during both the acute and chronic stages of infection and more rapid development of granulomas, with greater lung involvement and distinctive cellularity.

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“…This function is achieved by virtue of the size and strong negative charge of the extracellular domain. [15][16][17][18] During leukocyte activation, CD43 expression is dramatically down-regulated, allowing intercellular interactions mediated by molecules such as the ␤ 2 integrins. Intercellular interactions are also actively facilitated by CD43, which, due to changes in glycosylation, switches from being an antiadhesion to a proadhesion molecule.…”

Section: Introductionmentioning

confidence: 99%

hnRNP-K and Purα act together to repress the transcriptional activity of the CD43 gene promoter

Silva

Bharti

Shelley

2002

Blood

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CD43 is an abundant, heavily glycosylated molecule expressed specifically on the surface of leukocytes and platelets. When leukocytes are at rest, CD43 acts to prevent both homotypic and heterotypic interactions. However, during leukocyte activation CD43 expression is repressed, facilitating the intercellular contact required for chemotaxis, phagocytosis, aggregation, adhesion to endothelium, and transendothelial migration. Consequently, CD43 repression plays a vital role both in innate and acquired immunity. Here we report that a dramatic down-regulation of CD43 mRNA levels occurs during activation of the leukocytic cell line K562. This repression coincides with repression of the transcriptional activity of the CD43 gene promoter. We have determined that heterogeneous nuclear ribonucleopro- IntroductionCD43 is a heavily glycosylated transmembrane molecule that plays a critical role in leukocyte activation and adhesion. [1][2][3] The importance of CD43 is demonstrated by 2 immunodeficiency diseases, Wiskott-Aldrich syndrome (WAS) and the early stages of HIV infection. [4][5][6][7][8][9] The etiology of both diseases involves the development of defects in CD43. Patients with WAS, which is an X chromosome-linked, recessive disorder, express defective CD43 on the surface of their T lymphocytes. Affected males are subject to recurring opportunistic infections and do not respond to carbohydrate antigens, reflecting defects in T lymphocyte function. In addition, patients suffer from eczema and thrombocytopenia with platelets of reduced size and function. With regard to HIV infection, the finding that all affected individuals have circulating anti-CD43 antibodies has led to the suggestion that these autoantibodies contribute to severe immunodeficiency. 8 CD43 is composed of 381 amino acids divided between a 235-residue extracellular region, a 23-residue transmembrane region, and a 123-amino acid C-terminal intracellular region. 10,11 The extracellular region contains approximately 84 sialylated O-linked carbohydrate units and appears by electron microscopy to be a rodlike structure extending 45 nm from the cell surface. 12 Comparison of the rat, mouse, and human sequences indicates that the intracellular domain has been highly conserved during evolution, suggesting a critical function. The intracellular domain anchors CD43 to the cytoskeleton by binding actin, ezrin, and moesin. 13,14 When leukocytes are at rest, CD43 maintains their circulation within the bloodstream by preventing intercellular adhesion. This function is achieved by virtue of the size and strong negative charge of the extracellular domain. [15][16][17][18] During leukocyte activation, CD43 expression is dramatically down-regulated, allowing intercellular interactions mediated by molecules such as the ␤ 2 integrins. Intercellular interactions are also actively facilitated by CD43, which, due to changes in glycosylation, switches from being an antiadhesion to a proadhesion molecule. [19][20][21][22][23][24][25][26][27][28] The proadhesive function of C...

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Disregulation of leukosialin (CD43, Ly48, sialophorin) expression in the B-cell lineage of transgenic mice increases splenic B-cell number and survival.

Cited by 54 publications

References 53 publications

Overexpression of leukocyte marker CD43 causes activation of the tumor suppressor proteins p53 and ARF

Overexpression of leukocyte marker CD43 causes activation of the tumor suppressor proteins p53 and ARF

CD43 Is Required for Optimal Growth Inhibition of Mycobacterium tuberculosis in Macrophages and in Mice

hnRNP-K and Purα act together to repress the transcriptional activity of the CD43 gene promoter

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