Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-γ release by acetylcholine receptor-specific T cells

Mathilde A. Poussin; Claudette L. Fuller; Elzbieta Goluszko; Victor E. Reyes; Vivian L. Braciale; Premkumar Christadoss

doi:10.1016/S0165-5728(02)00425-3

Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-γ release by acetylcholine receptor-specific T cells

Mathilde A. Poussin
, Claudette L. Fuller
, Elzbieta Goluszko
, Victor E. Reyes
, Vivian L. Braciale
, Premkumar Christadoss

Pediatrics

Research output: Contribution to journal › Article › peer-review

4 Scopus citations

Abstract

Class II MHC mutant bm12 mice have an increased resistance to experimental autoimmune myasthenia gravis (EAMG) compared to C57BL/6 mice. In vitro, this relative resistance was mainly associated with a reduced cytokine response to acetylcholine receptor (AChR) and its dominant pathogenic peptide α146-162, whereas the response to the epitope α111-126 remained intact. Calcium mobilization after stimulation of AChR-immune T cells with AChR or α146-162 peptide, but not α111-126 peptide, was decreased in bm12 compared to C57BL/6. Thus, the reduced incidence of clinical EAMG in bm12 is linked to lower IFN-γ and IL-10 release, and intracellular calcium mobilization by α146-162-specific T cells.

Original language	English (US)
Pages (from-to)	104-110
Number of pages	7
Journal	Journal of Neuroimmunology
Volume	134
Issue number	1-2
DOIs	https://doi.org/10.1016/S0165-5728(02)00425-3
State	Published - Jan 2003

Keywords

Antigen presentation
Autoimmunity
Class II MHC
Cytokines
Mouse model
Myasthenia gravis

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

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10.1016/S0165-5728(02)00425-3

Cite this

Poussin, M. A., Fuller, C. L., Goluszko, E., Reyes, V. E., Braciale, V. L., & Christadoss, P. (2003). Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-γ release by acetylcholine receptor-specific T cells. Journal of Neuroimmunology, 134(1-2), 104-110. https://doi.org/10.1016/S0165-5728(02)00425-3

Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-γ release by acetylcholine receptor-specific T cells. / Poussin, Mathilde A.; Fuller, Claudette L.; Goluszko, Elzbieta et al.
In: Journal of Neuroimmunology, Vol. 134, No. 1-2, 01.2003, p. 104-110.

Research output: Contribution to journal › Article › peer-review

Poussin, MA, Fuller, CL, Goluszko, E, Reyes, VE, Braciale, VL & Christadoss, P 2003, 'Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-γ release by acetylcholine receptor-specific T cells', Journal of Neuroimmunology, vol. 134, no. 1-2, pp. 104-110. https://doi.org/10.1016/S0165-5728(02)00425-3

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title = "Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-γ release by acetylcholine receptor-specific T cells",

abstract = "Class II MHC mutant bm12 mice have an increased resistance to experimental autoimmune myasthenia gravis (EAMG) compared to C57BL/6 mice. In vitro, this relative resistance was mainly associated with a reduced cytokine response to acetylcholine receptor (AChR) and its dominant pathogenic peptide α146-162, whereas the response to the epitope α111-126 remained intact. Calcium mobilization after stimulation of AChR-immune T cells with AChR or α146-162 peptide, but not α111-126 peptide, was decreased in bm12 compared to C57BL/6. Thus, the reduced incidence of clinical EAMG in bm12 is linked to lower IFN-γ and IL-10 release, and intracellular calcium mobilization by α146-162-specific T cells.",

keywords = "Antigen presentation, Autoimmunity, Class II MHC, Cytokines, Mouse model, Myasthenia gravis",

author = "Poussin, \{Mathilde A.\} and Fuller, \{Claudette L.\} and Elzbieta Goluszko and Reyes, \{Victor E.\} and Braciale, \{Vivian L.\} and Premkumar Christadoss",

note = "Funding Information: This work was supported by grants from the Myasthenia Gravis Foundation of America, the Muscular Dystrophy Association and the Association Fran{\c c}aise contre les Myopathies. Mathilde A. Poussin was successively an Association Fran{\c c}aise contre les Myopathies, Myasthenia Gravis Foundation of America, a McLaughlin Fellowship Fund postdoctoral fellow, and a Muscular Dystrophy Association development grant recipient. The authors are grateful to Mardelle Susman, MA for critically editing this manuscript.",

year = "2003",

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doi = "10.1016/S0165-5728(02)00425-3",

language = "English (US)",

volume = "134",

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AU - Fuller, Claudette L.

AU - Goluszko, Elzbieta

AU - Reyes, Victor E.

AU - Braciale, Vivian L.

AU - Christadoss, Premkumar

N1 - Funding Information: This work was supported by grants from the Myasthenia Gravis Foundation of America, the Muscular Dystrophy Association and the Association Française contre les Myopathies. Mathilde A. Poussin was successively an Association Française contre les Myopathies, Myasthenia Gravis Foundation of America, a McLaughlin Fellowship Fund postdoctoral fellow, and a Muscular Dystrophy Association development grant recipient. The authors are grateful to Mardelle Susman, MA for critically editing this manuscript.

PY - 2003/1

Y1 - 2003/1

N2 - Class II MHC mutant bm12 mice have an increased resistance to experimental autoimmune myasthenia gravis (EAMG) compared to C57BL/6 mice. In vitro, this relative resistance was mainly associated with a reduced cytokine response to acetylcholine receptor (AChR) and its dominant pathogenic peptide α146-162, whereas the response to the epitope α111-126 remained intact. Calcium mobilization after stimulation of AChR-immune T cells with AChR or α146-162 peptide, but not α111-126 peptide, was decreased in bm12 compared to C57BL/6. Thus, the reduced incidence of clinical EAMG in bm12 is linked to lower IFN-γ and IL-10 release, and intracellular calcium mobilization by α146-162-specific T cells.

AB - Class II MHC mutant bm12 mice have an increased resistance to experimental autoimmune myasthenia gravis (EAMG) compared to C57BL/6 mice. In vitro, this relative resistance was mainly associated with a reduced cytokine response to acetylcholine receptor (AChR) and its dominant pathogenic peptide α146-162, whereas the response to the epitope α111-126 remained intact. Calcium mobilization after stimulation of AChR-immune T cells with AChR or α146-162 peptide, but not α111-126 peptide, was decreased in bm12 compared to C57BL/6. Thus, the reduced incidence of clinical EAMG in bm12 is linked to lower IFN-γ and IL-10 release, and intracellular calcium mobilization by α146-162-specific T cells.

KW - Antigen presentation

KW - Autoimmunity

KW - Class II MHC

KW - Cytokines

KW - Mouse model

KW - Myasthenia gravis

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Suppressed clinical experimental autoimmune myasthenia gravis in bm12 mice is linked to reduced intracellular calcium mobilization and IL-10 and IFN-γ release by acetylcholine receptor-specific T cells

Abstract

Keywords

ASJC Scopus subject areas

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