Administration of Monoclonal Antibodies against Vascular Cell Adhesion Molecule-1/Very Late Antigen-4 Abrogates Predisposing Autoimmune Diabetes in NOD Mice

Tsukamoto, Kazuya; Yokono, Koichi; Amano, Kazutaka; Nagata, Michio; Yagi, Norio; Tominaga, Yoshihiro; Moriyama, Hiroaki; Miki, Masaki; Okamoto, Nobuhiko; Yoneda, Ryoji; Inoue, Yoshio; Yagita, Hideo; Okumura, Ko; Kasuga, Masato

doi:10.1006/cimm.1995.1205

Cited by 29 publications

(14 citation statements)

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“…Consistent with our observation, the adoptive transfer of diabetes in the NOD mouse can be delayed by treatment with anti-VCAM-1 (24,56). Therefore, the blockade of VCAM-1 may represent a potential therapeutic treatment for T1DM.…”

Section: Discussionsupporting

confidence: 85%

Dynamic interaction between T cell-mediated β-cell damage and β-cell repair in the run up to autoimmune diabetes of the NOD mouse

Vukkadapu¹,

Belli²,

Ishii³

et al. 2005

Physiological Genomics

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Section: Discussionsupporting

confidence: 85%

Dynamic interaction between T cell-mediated β-cell damage and β-cell repair in the run up to autoimmune diabetes of the NOD mouse

Vukkadapu¹,

Belli²,

Ishii³

et al. 2005

Physiological Genomics

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“…These models include spontaneously occurring diabetes in the NOD mouse (30), asthma (31), and conjunctivitis (32). VLA-4 also has been shown to play an integral part in allograft rejection (33), and Ab's targeting it and other adhesion molecules have been the focus of attempts to induce immunosuppression in transplant recipients (34).…”

Section: Figurementioning

confidence: 99%

Discordant effects of anti–VLA-4 treatment before and after onset of relapsing experimental autoimmune encephalomyelitis

Theien¹,

Vanderlugt²,

Eagar³

et al. 2001

J. Clin. Invest.

109

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“…Seven-day-old NOD mice were injected intraperitoneally with 500 m g of either R1-2; anti-a4-integrin and M/K2; anti-vascular cell adhesion molecule-1 (VCAM-1) mAbs [13] or KAT-1; anti-intercellular adhesion molecule-1 (ICAM-1) and KBA; anti-leukocyte function-associated antigen-1 (LFA-1) mAbs [14] ) were preincubated with 10 m g/ml relevant mAbs for 30 min at 4°C before injection into corresponding mAbspretreated NOD recipients. Diabetic incidence was monitored up to 7 days after transfer and pancreatic insulitis of four mice in each group was evaluated at 3 days after transfer.…”

Section: Adoptive Transfer Of Diabetes By Cd8 T-cell Clonesmentioning

confidence: 99%

“…Diabetic incidence was monitored up to 7 days after transfer and pancreatic insulitis of four mice in each group was evaluated at 3 days after transfer. The severity of insulitis was assessed by using the scoring system as follows [13,14]: 0) normal islets; 1) mononuclear cell infiltration in less than 25 % of the islets; 2) 25-50 % of the islet infiltrated; 3) over 50 % infiltrated; 4) small retracted islets with few mononuclear cells.…”

Section: Adoptive Transfer Of Diabetes By Cd8 T-cell Clonesmentioning

confidence: 99%

CD8 cytotoxic T-cell clone rapidly transfers autoimmune diabetes in very young NOD and MHC class I-compatible scid mice

et al. 1997

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Nonobese diabetic (NOD) mice spontaneously develop an autoimmune diabetes resembling human insulin-dependent diabetes mellitus (IDDM). Several lines of evidence suggest that T cells are responsible for mononuclear cell infiltration into the islets (insulitis) and destruction of beta cells in NOD mice. Disease transfer studies have shown that both splenic CD4 and CD8 T cells from diabetic NOD mice are necessary to transfer diabetes to newborn or sublethally irradiated NOD mice [1, 2] and islet-specific CD4 and CD8 T-cell clones are both required before significant insulitis develops in irradiated NOD mice [3]. However, islet-specific CD4 T-cell clones have been found to cause diabetes when injected into unmanipulated young NOD mice [4] or NOD F1 mice [5]. In addition, CD4 T cells from diabetic NOD donors have also been shown to transfer disease into NOD-severe combined immunodeficient (scid) mice

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Administration of Monoclonal Antibodies against Vascular Cell Adhesion Molecule-1/Very Late Antigen-4 Abrogates Predisposing Autoimmune Diabetes in NOD Mice

Cited by 29 publications

References 0 publications

Dynamic interaction between T cell-mediated β-cell damage and β-cell repair in the run up to autoimmune diabetes of the NOD mouse

Dynamic interaction between T cell-mediated β-cell damage and β-cell repair in the run up to autoimmune diabetes of the NOD mouse

Discordant effects of anti–VLA-4 treatment before and after onset of relapsing experimental autoimmune encephalomyelitis

CD8 cytotoxic T-cell clone rapidly transfers autoimmune diabetes in very young NOD and MHC class I-compatible scid mice

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