Adhesion molecules in human islet beta-cells. De novo induction of ICAM-1 but not LFA-3

Vives, M.; Soldevila, G.; Alcalde, L.; Lorenzo, C.; Somoza, N.; Pujol-Borrell, R.

doi:10.2337/diabetes.40.11.1382

Cited by 17 publications

(9 citation statements)

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“…Vives et al (18) have reported that cultured human islets will express ICAM-1 in the absence of added stimuli. We have confirmed this induction by assaying ICAM-1 mRNA, which appears approximately 6 h after initiation of the culture.…”

Section: Discussionmentioning

confidence: 98%

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Control of Islet Intercellular Adhesion Molecule-1 Expression by Interferon-α and Hypoxia

Chakrabarti

Huang²,

Beck³

et al. 1996

Diabetes

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The ability of interferon-alpha (IFN-alpha) to induce the adhesion molecules that characterize the islets of patients with type I diabetes has been investigated. We have found that all tested recombinant IFN-as will induce major histocompatibility complex (MHC) class I on arterial endothelial cells. Some but not all IFN-as will induce intercellular adhesion molecule-1 (ICAM-1). However, there is only a transient and modest increase in VCAM on arterial endothelial cells. IFN-alpha has very little effect on endothelial MHC class II expression but will induce these proteins on monocytes. Thus, there is a close concordance between the biological actions of IFN-alpha and the appearance of those adhesion molecules induced in the islets of patients with type I diabetes. IFN-alpha is also produced in normal human islets during short-term cultures, probably as a result of the ischemia present at the center of the islet. This induction of IFN-alpha by hypoxia may explain the previously reported spontaneous induction of ICAM-1 in human islets and may also be a contributing factor to the failure of islet grafts.

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Section: Discussionmentioning

confidence: 98%

“…The expression of ICAM-1 may also be influenced by factors other than cytokines. It has been reported that ICAM-1 is spontaneously expressed by human islets put into culture (18) and ICAM-1 is induced on endothelial cells by re-oxygenation after hypoxia (19).…”

mentioning

confidence: 99%

Control of Islet Intercellular Adhesion Molecule-1 Expression by Interferon-α and Hypoxia

Chakrabarti

Huang²,

Beck³

et al. 1996

Diabetes

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“…Other potential APC include nonlymphoid cells such as capillary endothelium and 6 cells, which have been shown to be inducible for class I1 expression in the presence of cytokines [14][15][16]. As shown in Fig.…”

Section: Infiltrating Cells In Adoptively Transferred Diabetesmentioning

confidence: 96%

Antigen‐presenting cells in adoptively transferred and spontaneous autoimmune diabetes

Reilly

Scott

et al. 1993

Eur J Immunol

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Histological techniques were used to identify antigen-presenting cells (APC) in adoptively transferred diabetes in NOD mice and Ins-HA transgenic mice, and in spontaneously diabetic NOD mice. In adoptively transferred disease, CD4+ T cells and F4/80+ macrophages dominated early infiltrates. By contrast, in spontaneously developing diabetes in NOD mice, lymphocytic infiltrates appeared to be well organized around a network of VCAM-1+ NLDC-145+ ICAM-1+ dendritic cells. Thus, the primary APC spontaneous autoimmune disease appears to be the strongly stimulatory dendritic cell rather than the normally resident macrophage. Next, we used chimeric animals to demonstrate that insulitis and diabetes could occur even when responding T cells were unable to recognize islet-specific antigen directly on beta cells. Altogether, the results demonstrate that immune-mediated damage does not require direct contact between CD4+ T cells and beta cells. Moreover, despite the induction of ICAM-1, VCAM-1, and class II on vascular endothelium near islet infiltrates, these experiments show that recruitment of lymphocytes occurs even when antigen presentation is not possible on vascular endothelium.

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“…To assess the expression of TAP-1 in the different islet cell types by IFL, we have followed variations of already described protocols (31) combining an affinity-purified rabbit anti-TAP-1 antiserum (R.Ring 4c, Dr. P. Cresswell, New Haven, CT) with monoclonal antibodies (MoAbs) to insular antigens and to HLA molecules. R.Ring 4c is a rabbit antiserum derived against a peptide corresponding to the COOH-terminal 14 amino acids of TAP-1 and recognizes this molecule in native configuration (32).…”

Section: Methodsmentioning

confidence: 99%

Expression of Transporter Associated With Antigen Processing–1 in the Endocrine Cells of Human Pancreatic Islets: Effect of Cytokines and Evidence of Hyperexpression in IDDM

Vives-Pi

Armengol²,

Alcalde³

et al. 1996

Diabetes

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A possible role of transporter associated with antigen processing (TAP)-1 in the pathogenesis of IDDM has been investigated by examining the level of TAP-1 expression in the islets of IDDM pancreas and by studying in vitro the effect of interferon (IFN)-gamma, IFN-alpha, and tumor necrosis factor-alpha in TAP-1 expression by cultured islet cells. A remarkable hyperexpression of TAP-1 has been found in the endocrine cells (beta and non-beta) of IDDM islets, which constitutes first evidence of hyperexpression of this molecule in the target organ of an autoimmune disease. TAP-1 hyperexpression correlated clearly with HLA class I hyperexpression but only very partially with HLA class II ectopic expression. IFN-gamma and IFN-alpha, both cytokines putatively implicated in IDDM pathogenesis, were capable of inducing TAP-1 protein (as assessed by immunofluorescence flow cytometry) and message (by Northern blot analysis and reverse transcription polymerase chain reaction). These findings suggest that under the influence of cytokines (most probably IFN-alpha) beta-cells may express in their surface a high density of HLA class I-peptide complexes that may facilitate their recognition and lysis by low-affinity CD8+ T-cells.

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Adhesion molecules in human islet beta-cells. De novo induction of ICAM-1 but not LFA-3

Cited by 17 publications

References 0 publications

Control of Islet Intercellular Adhesion Molecule-1 Expression by Interferon-α and Hypoxia

Control of Islet Intercellular Adhesion Molecule-1 Expression by Interferon-α and Hypoxia

Antigen‐presenting cells in adoptively transferred and spontaneous autoimmune diabetes

Expression of Transporter Associated With Antigen Processing–1 in the Endocrine Cells of Human Pancreatic Islets: Effect of Cytokines and Evidence of Hyperexpression in IDDM

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