ICAM‐1 tissue overexpression associated with increased serum levels of its soluble form in Hodgkin's disease

Abstract

We investigated ICAM-1/CD54 tissue immunoreactivity and serum levels of its soluble form (sICAM-1) in patients with Hodgkin's disease (HD) at diagnosis. ICAM-1 was strongly expressed in involved tissues, and sICAM-1 serum levels were higher in HD (79 patients) than in controls (P < 0.01), and in patients with more advanced or more active disease (stages III + IV vI + II: P = 0.002; stage 'B' v 'A': P < 0.0001; 'bulky' disease v non-'bulky': P = 0.042). We suggest that tissue ICAM-1 overexpression leading to increase of circulating sICAM-1 may interfere with the lymphocyte adhesion machinery thus contributing to the well-known immune derangement of HD.

Expression of intercellular adhesion molecule 1 (ICAM‐1) in childhood acute lymphoblastic leukaemia: correlation with clinical features and outcome

“…In vitro data suggest a role for CD54 and CD58 in mediating cytolytic activity towards tumour cells (Schirren et al, 1992;Archimbaud et al, 1994). Leukaemic blasts might acquire a selective advantage by down-regulating or shedding (Gruss et al, 1993;Pizzolo et al, 1993), Wilms tumour (Pui et al, 1993a), malignant melanoma (Altomonte et al, 1992) and chronic lymphocytic leukaemia (CLL) (Christiansen et al, 1994). However, it has not yet been defined whether serum levels reflect shedding of CD54 from tumour cells or just a higher tumour burden.…”

Epstein–Barr virus expression in Hodgkin’s disease in relation to patient characteristics, serum factors and blood lymphocyte function

“…Furthermore, the CD30 ligand (CD30L), a member of the tumour necrosis factor/nerve growth factor (TNF/NGF) superfamily is known to up-regulate CD54 expression by CD30+ cultured HRS cells, and to increase shedding of surface-bound CD54 . Pizzolo et al (1993) have also reported that an increased expression of CD54 in HD tissue was associated with high levels of serum sCD54, and with more advanced clinical stage and the presence of constitutional symptoms and bulky disease. In a previous study, elevated sCD54 values were observed in patients with high age, advanced disease, constitutional symptoms, lymphocytic depletion histopathology, decreased remission rate and 5-year survival and abnormal lymphocyte function .…”

Matrix metalloproteinase 9 (MMP-9/gelatinase B) proteolytically cleaves ICAM-1 and participates in tumor cell resistance to natural killer cell-mediated cytotoxicity

“…Similar to their normal hematopoietic and epithelial counterparts, leukemic cells and carcinomas express ICAM-1, which may be predicted to facilitate targeting by cytotoxic cells. However, ICAM-1 is shed from the surface of tumor cells, and serum levels of soluble ICAM-1 have even been proposed to provide an indicator of tumor burden (Grothey et al, 1998;Harning et al, 1991;Pizzolo et al, 1993). More to the point, shedding of ICAM-1 has been observed to inhibit cell mediated cytotoxicity and provide primary tumor cells as well as tumor cell lines with a mechanism of defense against cytolytic T cells and NK cells (Altomonte et al, 1993;Becker and Brocker, 1995;Becker et al, 1991;Fonsatti et al, 1997;Sanchez-Rovira et al, 1998).…”