Partial inhibition of AT-EAE by an antibody to ICAM-1: Clinico-histological and MRI studies

Morrissey, S. P.; Deichmann, R.; Syha, Jutta; Simonis, Claudia; Zettl, Uwe K.; Archelos, Juan J.; Jung, Stefan; Stodal, Horst; Lassmann, Hans; Toyka, Klaus V.; Haase, Axel; Hartung, Hans‐Peter

doi:10.1016/0165-5728(96)00064-1

Cited by 33 publications

(12 citation statements)

References 43 publications

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“…The results of this study clearly demonstrate that ICAM-1 plays a central role in the development of demyelinating disease. Our findings contrast with several previous EAE studies using inhibitory anti-ICAM-1 Abs or Icam1 tm1Bay mice (25)(26)(27)(28)(29)(30)(31). At least for the Ab studies, these contrasting findings may be due to a number of reasons, including differential Ab specificity, insufficient dosage, differences in the timing of Ab delivery, and methodological differences in the induction or characterization of EAE.…”

Section: Discussioncontrasting

confidence: 56%

“…Most reports have described results using inhibitory ICAM-1 mAbs to block interactions of this adhesion molecule with its ligands. Although several of these studies have shown a protective outcome in active EAE (25)(26)(27), an almost equal number have reported no protection or increased severity of disease (28 -30). In contrast, loss, or inhibition of the ICAM-1 ligands LFA-1 and Mac-1 in EAE models have, in most cases, shown reduction in clinical severity and partial protection against the development of CNS inflammation.…”

Section: Ultiple Sclerosis (Ms)mentioning

confidence: 99%

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Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis

Bullard¹,

Hu²,

Schoeb³

et al. 2007

The Journal of Immunology

125

103

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Many members of the Ig superfamily of adhesion molecules, such as ICAM-1 and VCAM-1, have been implicated in the pathogenesis of multiple sclerosis. Although it is well-established that VCAM-1/VLA-4 interactions can play important roles in mediating CNS inflammatory events in multiple sclerosis patients and during the development of experimental allergic encephalomyelitis (EAE), the contributions of ICAM-1 are poorly understood. This is due in large part to conflicting results from Ab inhibition studies and the observation of exacerbated EAE in ICAM-1 mutant mice that express a restricted set of ICAM-1 isoforms. To determine ICAM-1-mediated mechanisms in EAE, we analyzed ICAM-1 null mutant mice (ICAM-1null), which express no ICAM-1 isoforms. ICAM-1null mice had significantly attenuated EAE characterized by markedly reduced spinal cord T cell infiltration and IFN-γ production by these cells. Adoptive transfer of Ag-restimulated T cells from wild-type to ICAM-1null mice or transfer of ICAM-1null Ag-restimulated T cells to control mice failed to induce EAE. ICAM-1null T cells also showed reduced proliferative capacity and substantially reduced levels of IFN-γ, TNF-α, IL-4, IL-10, and IL-12 compared with that of control T cells following myelin oligodendrocyte glycoprotein 35–55 restimulation in vitro. Our results indicate that ICAM-1 expression is critical on T cells and other cell types for the development of demyelinating disease and suggest that expression of VCAM-1 and other adhesion molecules cannot fully compensate for the loss of ICAM-1 during EAE development.

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Section: Discussioncontrasting

confidence: 56%

Section: Ultiple Sclerosis (Ms)mentioning

confidence: 99%

Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis

Bullard¹,

Hu²,

Schoeb³

et al. 2007

The Journal of Immunology

125

103

View full text Add to dashboard Cite

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“…Antibodies to ICAM-1 (Archelos et al, 1993;Kobayashi et al, 1995;Kawai et al, 1996;Morrissey et al, 1996) or to a4ßl (Yednock et al, 1992) have been shown to lessen the severity of EAE. Treatment of Lewis rats with antibody to ICAM-1 resulted in a reduced severity of EAE that was associated with diminished infiltration of leukocytes into the CNS (Archelos et al, 1993;Morrissey et al, 1996). Intrathecally administered ICAM-1 antibody also suppressed EAE in Lewis rats (Kawai et al, 1996).…”

mentioning

confidence: 99%

“…ICAM-i is a ligand for the ß2-integrins LFA-1 (CD11a/CD18) and Mac-i (CD11b/CD18) that are found on the surface of granulocytes and lymphocytes (Diamond et al, 1991). VCAM-1 interacts with the integrins a4ß1 and the blood-brain barrier and migration of T cells into the CNS (Morrissey et al, 1996). A similar impairment in leukocyte migration into the CNS was demonstrated in adoptively transferred EAE in Lewis rats treated with antibody to a4/31 (Yednock et al, 1992).…”

mentioning

confidence: 99%

Elevation of Cyclic AMP Levels in Astrocytes Antagonizes Cytokine‐Induced Adhesion Molecule Expression

Ballestas

Benveniste

1997

Journal of Neurochemistry

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Abstract:We have examined the effect of elevating cyclic AMP levels on cytokine-mediated enhancement of intercellular adhesion molecule-i (ICAM-i) and vascular cell adhesion molecule-i (VCAM-i) gene expression by astrocytes. Treatment of astrocytes with the cyclic AMP mimetic dibutyryl-cyclic AMP, or the agonists norepinephrine, forskolin, prostaglandin E 2, and cholera toxin alone had no effect on ICAM-i or VCAM-i mRNA gene expression. However, elevating cyclic AMP levels within the cells by these agents suppressed interleukin-i ß-and tumor necrosis factor-a-induced adhesion molecule expression at both the mRNA and protein levels. The phosphodiesterase type IV inhibitor, rolipram, was able to potentiate the inhibitory effect of forskolin on ICAM-i and VCAM-i gene expression. Inhibition of tumor necrosis factor-a-induced VCAM-i mRNA levels by forskolin was partially due to enhanced degradation of VCAM-i message, whereas the decay rates of tumor necrosis factora-induced ICAM-i message and interleukin-iß-induced ICAM-i /VCAM-i message were not affected by forskolin treatment. These results demonstrate that the pathways used by interleukin-iß and tumor necrosis factor-a to induce adhesion molecule expression are antagonized by cyclic AMP-dependent protein kinase-mediated signaling pathways.

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“…The entry of activated T cells into tissue compartments is a process governed by both integrin-mediated adhesions as well as chemokine-mediated migration. Very late Ag-4 (VLA-4) (5, 6), LFA-1 (7), and ICAM-1 (8) have all been demonstrated as important adhesion molecules regulating disease progression.…”

mentioning

confidence: 99%

CXCL10 (IFN-γ-Inducible Protein-10) Control of Encephalitogenic CD4+ T Cell Accumulation in the Central Nervous System During Experimental Autoimmune Encephalomyelitis

Fife

Kennedy

Paniagua

et al. 2001

The Journal of Immunology

243

186

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Experimental autoimmune encephalomyelitis (EAE) is a CD4+ Th1-mediated demyelinating disease of the CNS that serves as a model for multiple sclerosis. A critical event in the pathogenesis of EAE is the entry of both Ag-specific and Ag-nonspecific T lymphocytes into the CNS. In the present report, we investigated the role of the CXC chemokine CXCL10 (IFN-γ-inducible protein-10) in the pathogenesis of EAE. Production of CXCL10 in the CNS correlated with the development of clinical disease. Administration of anti-CXCL10 decreased clinical and histological disease incidence, severity, as well as infiltration of mononuclear cells into the CNS. Anti-CXCL10 specifically decreased the accumulation of encephalitogenic PLP139–151 Ag-specific CD4+ T cells in the CNS compared with control-treated animals. Anti-CXCL10 administration did not affect the activation of encephalitogenic T cells as measured by Ag-specific proliferation and the ability to adoptively transfer EAE. These results demonstrate an important role for the CXC chemokine CXCL10 in the recruitment and accumulation of inflammatory mononuclear cells during the pathogenesis of EAE.

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Partial inhibition of AT-EAE by an antibody to ICAM-1: Clinico-histological and MRI studies

Cited by 33 publications

References 43 publications

Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis

Intercellular Adhesion Molecule-1 Expression Is Required on Multiple Cell Types for the Development of Experimental Autoimmune Encephalomyelitis

Elevation of Cyclic AMP Levels in Astrocytes Antagonizes Cytokine‐Induced Adhesion Molecule Expression

CXCL10 (IFN-γ-Inducible Protein-10) Control of Encephalitogenic CD4+ T Cell Accumulation in the Central Nervous System During Experimental Autoimmune Encephalomyelitis

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