Costimulatory signal blockade in murine relapsing experimental autoimmune encephalomyelitis.

M Schaub; Shohreh Issazadeh-Navikas; T H Stadlbauer; R Peach; M H Sayegh; S J Khoury

Costimulatory signal blockade in murine relapsing experimental autoimmune encephalomyelitis.

M Schaub, Shohreh Issazadeh-Navikas, T H Stadlbauer, R Peach, M H Sayegh, S J Khoury

35 Citations (Scopus)

Abstract

Blockade of the CD28-B7 or CD40L-CD40 T cell costimulatory signals prevents induction of experimental autoimmune encephalomyelitis (EAE). However, the effect of simultaneous blockade of these signals in EAE is unknown. We show that administration of either MR1 (to block CD40L) or CTLA4Ig (to block B7) after immunization or after the first attack protects from EAE. Treatment with a combination of CTLA4Ig and MR1 provides additive protection, and is associated with complete absence of mononuclear cell infiltrates in the central nervous system, and marked suppression of proliferation of primed T cells in the periphery. Selective B7-1 blockade did not protect from EAE. These observations have implications for therapy of autoimmune diseases.

Original language	English
Journal	Journal of Neuroimmunology
Volume	96
Issue number	2
Pages (from-to)	158-66
Number of pages	8
ISSN	0165-5728
Publication status	Published - 1999

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title = "Costimulatory signal blockade in murine relapsing experimental autoimmune encephalomyelitis.",

abstract = "Blockade of the CD28-B7 or CD40L-CD40 T cell costimulatory signals prevents induction of experimental autoimmune encephalomyelitis (EAE). However, the effect of simultaneous blockade of these signals in EAE is unknown. We show that administration of either MR1 (to block CD40L) or CTLA4Ig (to block B7) after immunization or after the first attack protects from EAE. Treatment with a combination of CTLA4Ig and MR1 provides additive protection, and is associated with complete absence of mononuclear cell infiltrates in the central nervous system, and marked suppression of proliferation of primed T cells in the periphery. Selective B7-1 blockade did not protect from EAE. These observations have implications for therapy of autoimmune diseases.",

author = "M Schaub and Shohreh Issazadeh-Navikas and Stadlbauer, {T H} and R Peach and Sayegh, {M H} and Khoury, {S J}",

note = "Keywords: Animals; Antigens, CD; Antigens, CD28; Antigens, CD80; Antigens, Differentiation; CD40 Ligand; Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Synergism; Encephalomyelitis, Autoimmune, Experimental; Female; Immunoconjugates; Immunosuppressive Agents; Membrane Glycoproteins; Mice; Myelin Basic Proteins; Recurrence; Signal Transduction; T-Lymphocytes; Time Factors",

year = "1999",

language = "English",

volume = "96",

pages = "158--66",

journal = "Journal of Neuroimmunology",

issn = "0165-5728",

publisher = "Elsevier",

number = "2",

}

TY - JOUR

T1 - Costimulatory signal blockade in murine relapsing experimental autoimmune encephalomyelitis.

AU - Schaub, M

AU - Issazadeh-Navikas, Shohreh

AU - Stadlbauer, T H

AU - Peach, R

AU - Sayegh, M H

AU - Khoury, S J

N1 - Keywords: Animals; Antigens, CD; Antigens, CD28; Antigens, CD80; Antigens, Differentiation; CD40 Ligand; Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Synergism; Encephalomyelitis, Autoimmune, Experimental; Female; Immunoconjugates; Immunosuppressive Agents; Membrane Glycoproteins; Mice; Myelin Basic Proteins; Recurrence; Signal Transduction; T-Lymphocytes; Time Factors

PY - 1999

Y1 - 1999

N2 - Blockade of the CD28-B7 or CD40L-CD40 T cell costimulatory signals prevents induction of experimental autoimmune encephalomyelitis (EAE). However, the effect of simultaneous blockade of these signals in EAE is unknown. We show that administration of either MR1 (to block CD40L) or CTLA4Ig (to block B7) after immunization or after the first attack protects from EAE. Treatment with a combination of CTLA4Ig and MR1 provides additive protection, and is associated with complete absence of mononuclear cell infiltrates in the central nervous system, and marked suppression of proliferation of primed T cells in the periphery. Selective B7-1 blockade did not protect from EAE. These observations have implications for therapy of autoimmune diseases.

AB - Blockade of the CD28-B7 or CD40L-CD40 T cell costimulatory signals prevents induction of experimental autoimmune encephalomyelitis (EAE). However, the effect of simultaneous blockade of these signals in EAE is unknown. We show that administration of either MR1 (to block CD40L) or CTLA4Ig (to block B7) after immunization or after the first attack protects from EAE. Treatment with a combination of CTLA4Ig and MR1 provides additive protection, and is associated with complete absence of mononuclear cell infiltrates in the central nervous system, and marked suppression of proliferation of primed T cells in the periphery. Selective B7-1 blockade did not protect from EAE. These observations have implications for therapy of autoimmune diseases.

M3 - Journal article

C2 - 10337914

SN - 0165-5728

VL - 96

SP - 158

EP - 166

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

IS - 2

ER -

Costimulatory signal blockade in murine relapsing experimental autoimmune encephalomyelitis.

Abstract

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