Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis

Elzbieta Goluszko; Peter Hjelmström; Caishu Deng; Mathilde A. Poussin; Nancy H. Ruddle; Premkumar Christadoss

doi:10.1016/S0165-5728(00)00420-3

Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis

Elzbieta Goluszko
, Peter Hjelmström
, Caishu Deng
, Mathilde A. Poussin
, Nancy H. Ruddle
, Premkumar Christadoss

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

22 Scopus citations

Abstract

A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-α deficient (LT-α^-/-) mice compared to LT-α^+/+ mice when immunized with acetylcholine receptor. However, only a partial prevention of clinical EAMG incidence was observed in LT-β^-/- mice compared to LT-β^+/+ mice. LT-α^-/- and LT-β^-/- mice had lower mean titers of total IgG, IgG1, IgG2a and IgG2b and higher or equal mean titers of IgM anti-AChR antibodies compared to controls. Therefore, LT-α^-/- and LT-β^-/- AChR immunized mice are capable of mounting a primary (IgM) humoral immune response to AChR, but are less capable of switching to the pathogenic anti-AChR IgG isotypes. LT could play a significant role in the pathogenesis of myasthenia gravis.

Original language	English (US)
Pages (from-to)	109-118
Number of pages	10
Journal	Journal of Neuroimmunology
Volume	113
Issue number	1
DOIs	https://doi.org/10.1016/S0165-5728(00)00420-3
State	Published - Feb 1 2001
Externally published	Yes

Keywords

Acetylcholine receptors
Autoimmunity
Cytokines
Lymphotoxins
Myasthenia gravis
TNF receptors

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

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10.1016/S0165-5728(00)00420-3

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title = "Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis",

abstract = "A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-α deficient (LT-α-/-) mice compared to LT-α+/+ mice when immunized with acetylcholine receptor. However, only a partial prevention of clinical EAMG incidence was observed in LT-β-/- mice compared to LT-β+/+ mice. LT-α-/- and LT-β-/- mice had lower mean titers of total IgG, IgG1, IgG2a and IgG2b and higher or equal mean titers of IgM anti-AChR antibodies compared to controls. Therefore, LT-α-/- and LT-β-/- AChR immunized mice are capable of mounting a primary (IgM) humoral immune response to AChR, but are less capable of switching to the pathogenic anti-AChR IgG isotypes. LT could play a significant role in the pathogenesis of myasthenia gravis.",

keywords = "Acetylcholine receptors, Autoimmunity, Cytokines, Lymphotoxins, Myasthenia gravis, TNF receptors",

author = "Elzbieta Goluszko and Peter Hjelmstr{\"o}m and Caishu Deng and Poussin, \{Mathilde A.\} and Ruddle, \{Nancy H.\} and Premkumar Christadoss",

note = "Funding Information: The study was supported by Muscular Dystrophy Association and Association Fran{\c c}aise Contre les Myopathies (P.C.), NIH, CA ROI CA 16885 (NHR), and a fellowship from the Swedish Foundation for International Cooperation in Research and Higher Education (P.H.). M. Poussin is a consecutive postdoctoral fellow of Association Fran{\c c}aisc Contre les Myopathies, Osserman fellow of the MG Foundation of America, and James W. McLaughlin Foundation postdoctoral fellow. C. Deng was an Osserman fellow of MG Fountation and James W. McLaughlin Foundation postdoctoral fellow.",

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doi = "10.1016/S0165-5728(00)00420-3",

language = "English (US)",

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pages = "109--118",

journal = "Journal of Neuroimmunology",

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T1 - Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis

AU - Goluszko, Elzbieta

AU - Hjelmström, Peter

AU - Deng, Caishu

AU - Poussin, Mathilde A.

AU - Ruddle, Nancy H.

AU - Christadoss, Premkumar

N1 - Funding Information: The study was supported by Muscular Dystrophy Association and Association Française Contre les Myopathies (P.C.), NIH, CA ROI CA 16885 (NHR), and a fellowship from the Swedish Foundation for International Cooperation in Research and Higher Education (P.H.). M. Poussin is a consecutive postdoctoral fellow of Association Françaisc Contre les Myopathies, Osserman fellow of the MG Foundation of America, and James W. McLaughlin Foundation postdoctoral fellow. C. Deng was an Osserman fellow of MG Fountation and James W. McLaughlin Foundation postdoctoral fellow.

PY - 2001/2/1

Y1 - 2001/2/1

N2 - A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-α deficient (LT-α-/-) mice compared to LT-α+/+ mice when immunized with acetylcholine receptor. However, only a partial prevention of clinical EAMG incidence was observed in LT-β-/- mice compared to LT-β+/+ mice. LT-α-/- and LT-β-/- mice had lower mean titers of total IgG, IgG1, IgG2a and IgG2b and higher or equal mean titers of IgM anti-AChR antibodies compared to controls. Therefore, LT-α-/- and LT-β-/- AChR immunized mice are capable of mounting a primary (IgM) humoral immune response to AChR, but are less capable of switching to the pathogenic anti-AChR IgG isotypes. LT could play a significant role in the pathogenesis of myasthenia gravis.

AB - A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-α deficient (LT-α-/-) mice compared to LT-α+/+ mice when immunized with acetylcholine receptor. However, only a partial prevention of clinical EAMG incidence was observed in LT-β-/- mice compared to LT-β+/+ mice. LT-α-/- and LT-β-/- mice had lower mean titers of total IgG, IgG1, IgG2a and IgG2b and higher or equal mean titers of IgM anti-AChR antibodies compared to controls. Therefore, LT-α-/- and LT-β-/- AChR immunized mice are capable of mounting a primary (IgM) humoral immune response to AChR, but are less capable of switching to the pathogenic anti-AChR IgG isotypes. LT could play a significant role in the pathogenesis of myasthenia gravis.

KW - Acetylcholine receptors

KW - Autoimmunity

KW - Cytokines

KW - Lymphotoxins

KW - Myasthenia gravis

KW - TNF receptors

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UR - https://www.scopus.com/pages/publications/0035255040#tab=citedBy

U2 - 10.1016/S0165-5728(00)00420-3

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IS - 1

ER -

Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis

Abstract

Keywords

ASJC Scopus subject areas

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