Intercellular adhesion molecule 1 (ICAM-1) has a central role in cell-cell contact-mediated immune mechanisms.

Boyd, Andrew W.; Wawryk, SO; Burns, Gordon F.; Fecondo, John V.

doi:10.1073/pnas.85.9.3095

Cited by 274 publications

(167 citation statements)

References 24 publications

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“…De novo expression of ICAM-1 has been described on different cell types in inflammatory lesion during rejection, and on melanoma cells [41]. Experimental studies have also shown that antibodies against ICAM-1 inhibit leukocyte adhesion to endothelial cells, granulocyte migration through endothelium, and mixed lymphocyte reactions in vitro [42]. In addition, in vivo administration of antibodies raised against ICAM-1 reduced neutrophil infiltration into the inflamed lungs in the rabbit and protects the development of SAO-induced injury.…”

Section: Discussionmentioning

confidence: 99%

IL-6 knock-out mice exhibit resistance to splanchnic artery occlusion shock

Cuzzocrea

Sarro

Costantino

et al. 1999

Journal of Leukocyte Biology

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We used IL-6 knock-out (KO) mice to evaluate a possible role for IL-6 in the pathogenesis of splanchnic artery occlusion shock (SAO). SAO shock was induced by clamping both the superior mesenteric artery and the celiac trunk, followed by release of the clamp. There was a marked increase in the peroxynitrite formation in the plasma of the SAO-shocked IL-6 wild-type (WT) mice after reperfusion. Immunohistochemical examination demonstrated a marked increase in the immunoreactivity to nitrotyrosine in the necrotic ileum in shocked IL-6 WT mice. SAO-shocked WT mice developed a significant increase of tissue myeloperoxidase (MPO) and malondialdehyde (MDA) activity and marked histological injury to the distal ileum. SAO shock was also associated with a significant mortality (0% survival). Reperfused ileum tissue sections from SAO-shocked WT mice showed positive staining for P-selectin. Little specific staining was observed in sham-WT mice. Staining of ileum tissue obtained from sham-operated WT mice with anti-ICAM-1 antibody showed weak but diffuse staining, demonstrating that ICAM-1 is constitutively expressed. However, after SAO shock the staining intensity increased substantially in the ileum section from WT mice. Intensity and degree of Pselectin and ICAM-1 were markedly reduced in tissue section from SAO-shocked IL-6 KO mice. SAO-shocked IL-6 KO mice also show significant reduction of neutrophil infiltration into the reperfused intestine, as evidenced by reduced MPO activity, improved histological status of the reperfused tissues, reduced peroxynitrite formation, reduced MDA levels, and improved survival. In vivo treatment with anti-IL-6 significantly prevents the inflammatory process. Our results clearly demonstrate that IL-6 plays an important role in ischemia and reperfusion injury and allows the hypothesis that inhibition of IL-6 may represent a novel and possible strategy. Part of this effect may be due to inhibition of the expression of adhesion molecules and subsequent reduction of neutrophil-mediated cellular injury. J. Leukoc. Biol. 66: 471-480; 1999.

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Section: Discussionmentioning

confidence: 99%

IL-6 knock-out mice exhibit resistance to splanchnic artery occlusion shock

Cuzzocrea

Sarro

Costantino

et al. 1999

Journal of Leukocyte Biology

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“…13 CD54 is an important ligand for leukocytes and is believed to be involved in immune surveillance. 15,16 Intravenous administration of MAb against human CD54 (UV3) results in long-term survival in SCID mice injected with human myeloma cells. 17 Moreover, UV3 was also highly effective in treating mice with advanced tumors.…”

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confidence: 99%

Effect of an anti‐CD54 (ICAM‐1) monoclonal antibody (UV3) on the growth of human uveal melanoma cells transplanted heterotopically and orthotopically in SCID mice

Wang

Coleman

Pop

et al. 2005

Intl Journal of Cancer

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We have shown that administration of a novel anti-CD54 monoclonal antibody (UV3) results in long-term survival of SCID mice bearing human myeloma xenografts. Previous studies have demonstrated a link between the expression of CD54 and the progression of uveal melanoma. Our study assessed the expression of CD54 on 7 human uveal melanoma cell lines and 3 cell lines established from uveal melanoma metastases. In vivo studies examined the efficacy of systemic and local administration of UV3 antibody on the progression of uveal melanoma cells transplanted either heterotopically or orthotopically into SCID mice. Five of the 7 primary uveal melanoma cell lines and all 3 of the metastases cell lines expressed CD54. Intraperitoneal injection of either IgG or F(ab 0 ) 2 fragments of UV3 significantly inhibited the growth of subcutaneous and intraocular melanomas. Subconjunctival injection of either IgG or F(ab 0 ) 2 fragments of UV3 produced a significant reduction in the growth of intraocular melanomas, even if the antibody was administered after the appearance of intraocular tumors. The results indicate that both primary and metastatic human uveal melanoma cells express CD54. The marked inhibition of intraocular and subcutaneous uveal melanoma progression suggests that UV3 antibody is a promising therapeutic agent for further evaluation in patients with uveal melanoma. This is especially noteworthy, as no existing therapeutic modality prevents metastasis of uveal melanoma or prolongs the survival of patients with uveal melanoma. ' 2005 Wiley-Liss, Inc.Key words: anterior chamber; eye; CD54; immunotherapy; uveal melanoma Uveal melanoma is the most common intraocular malignancy in adults and occurs with a frequency of 6 to 7 cases per one million adults. 1 Although cutaneous and uveal melanomas share a neural crest origin, they differ significantly in their epidemiological, 2 cytogenetic 3 , metastatic 4-6 and immunological 4 characteristics. One of the remarkable differences between cutaneous and uveal melanomas is their metastatic behavior. Although skin melanomas metastasize to almost any organ, uveal melanoma displays a propensity to spread to the liver. Indeed, liver metastases are present in up to 95% of the patients who die from uveal melanomas. [7][8][9][10] Although there have been advances in the treatment of primary uveal melanomas, the 5-year survival rate for uveal melanoma patients has not improved in the past 30 years. 1,10 Moreover, no therapeutic modality prevents the metastasis of uveal melanoma or prolongs the survival of patients. 11 Studies have suggested a correlation between the expression of CD54 and the progression of skin and uveal melanomas. 12,13 Expression of CD54 was detected in 81-85% of human uveal melanoma specimens. 13,14 Reduced expression of CD54 in primary uveal melanomas has been associated with increased metastatic disease. 13 CD54 is an important ligand for leukocytes and is believed to be involved in immune surveillance. 15,16 Intravenous administration of MAb against human CD54 (U...

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“…Two adhesion events that are of particular interest are the interaction between ICAM-I (CD54) and C D l l d C D 1 8 complex, and between CD2 and leukocyte function-associated antigen 3 (LFA-3) (CD58), not only because of their demonstrated role in cell-to-cell adhesion (17)(18)(19), but also because of their ability to facilitate antigen presentation to T lymphocytes and cytolysis (20)(21)(22)(23). Therefore, w e used a quantitative in vitro cellular adhesion system t o examine the relative contributions of ICAM-1-CD1 ldCD18 and of CD2-LFA-3 to T lymphocyte adhesion to cytokine-activated human synovial fibroblasts.…”

Section: T Lymphocyte Adhesion To Human Synovial Fibroblastsmentioning

confidence: 99%

T Lymphocyte Adhesion to Human Synovial Fibroblasts. Role of Cytokines and the Interaction Between Intercellular Adhesion Molecule 1 and CD11a/CD18

Krzesicki

Fleming

Winterrowd

et al. 1991

Arthritis & Rheumatism

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We studied the adhesion of human peripheral blood T lymphocytes to human synovial fibroblasts stimulated with interferon-y (IFNy), tumor necrosis factor a (TNFcu), interleukin-lp (IL-lp), or combinations of these cytokines. T lymphocytes bound poorly to untreated human synovial fibroblasts. IFN y treatment resulted id the largest increase in adhesion, followed by TNFa and IL-1p. Combinations of IFNy + TNFa and IFNy + I L -l p had a synergistic effect on intercellular adhesion molecule 1 (ICAM-1) expression and adhesion. The increase in cellular adhesion induced by cytokines correlated with the up-regulation of the number of cells expressing ICAM-1 and the density of antigedcell. There was no synergistic effect on leukocyte functionassociated antigen 3 (LFA-3) or on HLA class I or class I1 antigen expression. Adhesion was only partially inhibited by anti-ICAM-1, anti-LFA-1, or anti-CD18. These findings suggest the existence of ICAM-1-independent and CDll/CDlS-independent adhesion mechanisms. Anti-LFA-3 was completely ineffective as an inhibitor of adhesion. There was no additive or synergistic advantage of using combinations of antibod-~

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Intercellular adhesion molecule 1 (ICAM-1) has a central role in cell-cell contact-mediated immune mechanisms.

Cited by 274 publications

References 24 publications

IL-6 knock-out mice exhibit resistance to splanchnic artery occlusion shock

IL-6 knock-out mice exhibit resistance to splanchnic artery occlusion shock

Effect of an anti‐CD54 (ICAM‐1) monoclonal antibody (UV3) on the growth of human uveal melanoma cells transplanted heterotopically and orthotopically in SCID mice

T Lymphocyte Adhesion to Human Synovial Fibroblasts. Role of Cytokines and the Interaction Between Intercellular Adhesion Molecule 1 and CD11a/CD18

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