The activation antigen BLAST-2, when shed, is an autocrine BCGF for normal and transformed B cells.

Swendeman, Steven; Thorley‐Lawson, David A.

doi:10.1002/j.1460-2075.1987.tb02412.x

Cited by 190 publications

(83 citation statements)

References 34 publications

(20 reference statements)

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“…Cheah et al (1986) were unable to find c-fgr transcripts in the EBV-negative BL cell lines which they studied, but we find that low levels are detectable in the EBV-negative parent cell lines BL2, BL31 and BL41. Many of the changes in cellular phenotype which accompany EBVconversion resemble changes seen during normal Blymphocyte activation, most strikingly the acquisition of cell surface markers such as CD23 and Blast-I (Swendeman & Thorley-Lawson, 1987). These results raise the possibility, therefore, that the c-fgr protein is involved in the pathway of normal B-lymphocyte activation, perhaps as part of a protein phosphorylation cascade which transduces signals leading to B-lymphocyte differentiation and proliferation.…”

Section: Discussionmentioning

confidence: 86%

“…The molecular mechanisms whereby signals at the B-lymphocyte cell surface generate changes in DNA and RNA synthesis are of considerable interest. B-lymphocyte activation is accompanied by the appearance of a range of cell surface molecules, such as CD23 and Blast-I (Swendeman & Thorley-Lawson, 1987), and it is probable that some of these activation markers represent receptors for growth and differentiation factors. It has been shown, for example, that a fragment of CD23 shed from the surface of activated Blymphocytes can act as an autocrine B cell growth factor for normal and transformed B-lymphocytes (Swendeman & Thorley-Lawson, 1987).…”

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confidence: 99%

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Structure and expression of c-fgr protooncogene mRNA in Epstein-Barr virus converted cell lines

Brickell

Patel²

1988

Br J Cancer

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Summary The c-fgr protooncogene is a member of the c-src family of tyrosine kinases. Expression of c-fgr was studied in a series of Epstein-Barr virus (EBV) negative Burkitt's lymphoma cell lines and their EBVconverted derivatives. Two transcripts, of 2.9kb and 3.5kb, were present at dramatically elevated levels following EBV-conversion.The structure of the c-fgr transcripts was studied by the isolation and nucleotide sequence analysis of cDNA clones. This indicated that the c-fgr protein encoded by the mature mRNA would contain 529 amino acids and have a molecular weight of approximately 58,000. The N-terminus of the predicted c-fgr protein has low amino acid homology with the N-termini of other members of this family of proteins, suggesting a cell specific function for the N-terminal domain. Analysis of the c-fgr cDNA clones also revealed the presence of alternative functional polyadenylation signals, although the use of these does not account for the size difference between the two major c-fgr transcripts.

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Section: Discussionmentioning

confidence: 86%

mentioning

confidence: 99%

Structure and expression of c-fgr protooncogene mRNA in Epstein-Barr virus converted cell lines

Brickell

Patel²

1988

Br J Cancer

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“…Alternatively, FceRII has recently been found to be identical with CD23, which is known as a B cell activation marker; accumulating evidence suggests that some soluble fragments of FcsRII display B cell growth factor activity (Swendeman & Thorley-Lawson, 1987). The reduced serum levels of soluble FceRII products in ATL patients may account for the hypogammaglobulinaemia, including IgE, seen in such cases.…”

Section: Discussionmentioning

confidence: 99%

Decreased serum levels of IgE and IgE-binding factors in individuals infected with HTLV-I

Matsumoto¹,

Miike²,

Mizoguchi³

et al. 1990

Clinical and Experimental Immunology

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SUMMARYThe cell surface expression of low-affinity Fc epsilon receptor (FCERII), which is identical to CD23, and the serum levels of IgE binding factors (IgE BFs), a soluble form of FceRII, and IgE were investigated in HTLV-I-infected individuals, and the results were compared with those for HTLV-Inegative controls. The occurrence of FceRII + mononuclear cells did not differ among the blood samples from the HTLV-I-infected groups; however, the levels of serum IgE BFs were significantly decreased (/*< 0-001) in patients with adult T cell leukaemia (ATL), compared with HTLV-Inegative controls. The serum IgE levels were also significantly decreased in these groups, including cases of ATL (P< 0-001) and HTLV-I-associated myelopathy (P<0-05), and HTLV-I carriers (/'<0-05), as compared with HTLV-I-negative controls. Since cases of strongyloidiasis or filariasis are frequently found among HTLV-I-infected individuals in Japan, these results may explain in part their defective defence mechanisms for parasites. The possible involvement of IgE BFs in the development of immune deficiency state in HTLV-I infection is also discussed.

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“…Immortalized B ceils also express cellular activation antigens consistent with their lymphoblastoid stage of differentiation. These include CD23 , which is upregulated by the EBNA 2 gene product (Wang et al, 1987) and is cleaved and shed from the cell surface acting as an autocrine growth factor for LCL (Swendeman & Thorley-Lawson, 1987). A heterogeneity in the response of B cells to EB virus infection has been noted based on their expression of CD23.…”

Section: Introductionmentioning

confidence: 99%

Immortalization of Epstein--Barr virus-infected CD23-negative B lymphocytes by the addition of B cell growth factor

Azim

Allday

Crawford

1990

Journal of General Virology

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Epstein-Barr (EB) virus-immortalized B lymphocytes coexpress the EB viral latent gene products (EB viral nuclear antigens 1 to 6, the latent membrane protein and the terminal protein gene products) and the cellular activation antigen CD23. Immortalized B cells can be separated from those which are infected but not immortalized on the basis of CD23 expression as early as 2 days after in vitro infection. In the present report we have confirmed these data, but show that if left in culture for 7 days after infection before separation the CD23-negative cells show a donor-related ability to become CD23-positive and immortalize. CD23-negative cells separated 2 days after infection can be induced to immortalize by the addition of low Mr B cell growth factor but not by the addition of recombinant interleukin 1, 4 or soluble CD23. At 2 to 3 days after infection the EB viral nuclear antigens 1, 2 and the high Mr species 3, 4 and 6, as well as the latent membrane protein can be detected in the CD23-positive fraction. In contrast at this time only nuclear antigens 1 and 2 could be detected in the CD23-negative fraction. This difference in gene expression may account for the inability of the CD23-negative fraction to immortalize. In the light of these observations the mechanism of viral persistence in vivo is discussed.

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The activation antigen BLAST-2, when shed, is an autocrine BCGF for normal and transformed B cells.

Cited by 190 publications

References 34 publications

Structure and expression of c-fgr protooncogene mRNA in Epstein-Barr virus converted cell lines

Structure and expression of c-fgr protooncogene mRNA in Epstein-Barr virus converted cell lines

Decreased serum levels of IgE and IgE-binding factors in individuals infected with HTLV-I

Immortalization of Epstein--Barr virus-infected CD23-negative B lymphocytes by the addition of B cell growth factor

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