Co‐Iigation of ICAM‐1 (CD54) and membrane IgM negatively affects B cell receptor signaling

Horssen, Martin van; Loman, Stoffer; Rijkers, Ger T.; Boom, Saskia E.; Bloem, Andries C.

doi:10.1002/eji.1830250126

Cited by 23 publications

(9 citation statements)

References 42 publications

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“…In addition, ICAM-1 modulates changes in intracellular Ca 2ϩ in Burkitt's lymphoma (10). These results suggest an active role for ICAM-1 in signal transduction.…”

mentioning

confidence: 75%

Sequences within Fibrinogen and Intercellular Adhesion Molecule-1 (ICAM-1) Modulate Signals Required for Mitogenesis

Gardiner¹,

D’Souza

1999

Journal of Biological Chemistry

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“…In addition, ICAM-1 modulates changes in intracellular Ca 2ϩ in Burkitt's lymphoma (10). These results suggest an active role for ICAM-1 in signal transduction.…”

mentioning

confidence: 75%

Sequences within Fibrinogen and Intercellular Adhesion Molecule-1 (ICAM-1) Modulate Signals Required for Mitogenesis

Gardiner¹,

D’Souza

1999

Journal of Biological Chemistry

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“…So far, no correlation has been found between expression of known adhesion molecules and susceptibility to induction of detachment in cell lines. B cell detachment could be induced in cell lines lacking PZintegrins (MTLM4, [26]), 61-integrin members (BJAB), CD31, CD44, CD61, CD73 and L-selectin (BJAB, MTLMd), CD23 and CD32 (MTLM4, [26]). Furthermore, a possible role of CD22 was unlikely since its lectin-like activity is independent of divalent cations such as Ca2+ and Mg2+ [27,28] and was ruled out by the inability of blocking antibody HB22-7 (kindly provided by Dr. Tom Tedder) to influence adhesion to activated HUVEC in our model system.…”

Section: Mhc Class 11-mediated Regulation Of Adhesion Of Normal and Nmentioning

confidence: 99%

Anti‐adhesive signals are mediated via major histocompatibility complex class II molecules in normal and neoplastic human B cells: Correlation with B cell differentiation stage

Ahsmann¹,

Boom²,

Lokhorst³

et al. 1997

Eur J Immunol

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We show that major histocompatibility complex (MHC) class II molecules on B cells transit signals which regulate adhesion in a negative manner. Engagement of MHC class II molecules with antibodies results in detachment of B cells previously bound to interferon-gamma-activated human umbilical cord venous endothelial cells. This process depends on metabolic energy, active signaling and protein tyrosine kinase activity. The adhesion pathway influenced by this signaling event is neuraminidase sensitive. The anti-adhesive signaling program is activated in B cell lines with a mature phenotype, e.g. normal B cells from spleen and tonsil. In contrast, cell lines with a pre-B cell phenotype and normal B cells from peripheral blood are refractory to MHC class II-mediated regulation of adhesion. These results extend to neoplastic cells from patients with lymphoproliferative diseases representing different stages of B cell maturation. These results suggest that MHC class II-mediated signals regulate B cell adhesion in a developmentally programmed fashion; this might have implications for clinical behavior of B cell malignancies.

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“…Antibody binding was visualized with enhanced chemoluminescence (Amersham) detection with hyperfilm ECL (Amersham) after incubation with a horseradish peroxidase (HRP)-conjugated secondary antibody (Dako). Membranes incubated with antiBcl-2 or anti-Ras were extensively washed in PBS and reprobed with anti-Bax (Dako) and anti-␣-actin (Sigma) or anti-␥-adaptin (Sigma) and anti-ICAM-1 (clone F7.11 35 ), respectively. The level of protein expression was determined by densitometry following normalization for ␣-actin expression.…”

Section: Western Blottingmentioning

confidence: 99%

The cholesterol lowering drug lovastatin induces cell death in myeloma plasma cells

et al. 2002

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Lovastatin is an irreversible inhibitor of HMG-CoA reductase and blocks the production of mevalonate, a critical compound in the production of cholesterol and isoprenoids. Isoprenylation of target proteins, like the GTP-binding protein Ras, is essential for their membrane localization and subsequent participation in intracellular signaling cascades. Lovastatin effectively decreased the viability of plasma cells from cell lines (n = 10) and myeloma patients' samples (n = 8) in a dose-and time-dependent way. Importantly, co-incubation of lovastatin with dexamethasone had a synergistic effect in inducing plasma cell cytotoxity. This effect was not the consequence of a change in the protein expression levels of Bcl-2 or Bax induced by lovastatin. The decrease in plasma cell viability was the result of induction of apoptosis and inhibition of proliferation. Mevalonate effectively reversed the cytotoxic and cytostatic effects of lovastatin in plasma cells. The cytotoxic activity of lovastatin was higher in Pgp expressing cell lines, but did not correlate with the multidrug resistance (MDR)-related proteins LRP, Bcl-2 and Bax. Lovastatin treatment resulted in a shift of Ras localization from the membrane to the cytosol that was reversed by mevalonate. The data presented in this paper warrant study of lovastatin alone or in combination with therapeutic drugs, in the treatment of myeloma patients.

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Co‐Iigation of ICAM‐1 (CD54) and membrane IgM negatively affects B cell receptor signaling

Cited by 23 publications

References 42 publications

Sequences within Fibrinogen and Intercellular Adhesion Molecule-1 (ICAM-1) Modulate Signals Required for Mitogenesis

Sequences within Fibrinogen and Intercellular Adhesion Molecule-1 (ICAM-1) Modulate Signals Required for Mitogenesis

Anti‐adhesive signals are mediated via major histocompatibility complex class II molecules in normal and neoplastic human B cells: Correlation with B cell differentiation stage

The cholesterol lowering drug lovastatin induces cell death in myeloma plasma cells

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