Literature DB >> 7544693

Antibodies against leukocyte function-associated antigen-1 and against intercellular adhesion molecule-1 together suppress the progression of experimental allergic encephalomyelitis.

Y Kobayashi1, K Kawai, H Honda, S Tomida, N Niimi, T Tamatani, M Miyasaka, Y Yoshikai.   

Abstract

We obtained the evidence that coadministration in vivo of mAbs against leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) suppressed the progression of experimental allergic encephalomyelitis (EAE) in rats. The suppressive effect in vivo of coadministration of the mAbs during the induction phase was not prominent, but the administration of these mAbs during the effector phase markedly suppressed the progression of clinical illness and prevented the infiltration of encephalitogenic cells into the central nervous system. However, administration of the mAb to LFA-1 alone or ICAM-1 alone did not show such suppressive effects. These findings suggest that LFA-1 and ICAM-1 are critically involved in the development of EAE and that the administration together of mAbs against adhesion molecules including LFA-1 and ICAM-1 might provide a new immunotherapeutic approach for the treatment of multiple sclerosis.

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Year:  1995        PMID: 7544693     DOI: 10.1006/cimm.1995.1173

Source DB:  PubMed          Journal:  Cell Immunol        ISSN: 0008-8749            Impact factor:   4.868


  9 in total

Review 1.  Regulation of experimental autoimmune encephalomyelitis by chemokines and chemokine receptors.

Authors:  Adam Elhofy; Kevin J Kennedy; Brian T Fife; William J Karpus
Journal:  Immunol Res       Date:  2002       Impact factor: 2.829

2.  Delta-like ligand 4 regulates central nervous system T cell accumulation during experimental autoimmune encephalomyelitis.

Authors:  Nathanael D Reynolds; Nicholas W Lukacs; Nancy Long; William J Karpus
Journal:  J Immunol       Date:  2011-07-25       Impact factor: 5.422

Review 3.  Antigen-specific blocking of CD4-specific immunological synapse formation using BPI and current therapies for autoimmune diseases.

Authors:  Prakash Manikwar; Paul Kiptoo; Ahmed H Badawi; Barlas Büyüktimkin; Teruna J Siahaan
Journal:  Med Res Rev       Date:  2011-03-23       Impact factor: 12.944

4.  Wallerian degeneration in ICAM-1-deficient mice.

Authors:  V I Vougioukas; S Roeske; U Michel; W Brück
Journal:  Am J Pathol       Date:  1998-01       Impact factor: 4.307

5.  p150/95 (CD11c/CD18) expression is required for the development of experimental autoimmune encephalomyelitis.

Authors:  Daniel C Bullard; Xianzhen Hu; Jillian E Adams; Trenton R Schoeb; Scott R Barnum
Journal:  Am J Pathol       Date:  2007-06       Impact factor: 4.307

6.  Structural modifications of ICAM-1 cyclic peptides to improve the activity to inhibit heterotypic adhesion of T cells.

Authors:  Bimo A Tejo; Usman S F Tambunan; Gennady Verkhivker; Teruna J Siahaan
Journal:  Chem Biol Drug Des       Date:  2008-06-11       Impact factor: 2.817

Review 7.  Pharmacological targeting of ICAM-1 signaling in brain endothelial cells: potential for treating neuroinflammation.

Authors:  Patric Turowski; Peter Adamson; John Greenwood
Journal:  Cell Mol Neurobiol       Date:  2005-02       Impact factor: 5.046

8.  CC chemokine receptor 2 is critical for induction of experimental autoimmune encephalomyelitis.

Authors:  B T Fife; G B Huffnagle; W A Kuziel; W J Karpus
Journal:  J Exp Med       Date:  2000-09-18       Impact factor: 14.307

9.  Human mesenchymal stem cells target adhesion molecules and receptors involved in T cell extravasation.

Authors:  Federica Benvenuto; Adriana Voci; Enrico Carminati; Francesca Gualandi; Gianluigi Mancardi; Antonio Uccelli; Laura Vergani
Journal:  Stem Cell Res Ther       Date:  2015-12-10       Impact factor: 6.832

  9 in total

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