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

Authors
Goluszko, E Hjelmstrom, P Deng, CS Poussin, MA Ruddle, NH Christadoss, P
Citation
E. Goluszko et al., Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis, J NEUROIMM, 113(1), 2001, pp. 109-118
Citations number
36
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROIMMUNOLOGY
ISSN journal
01655728 → ACNP
Volume
113
Issue
1
Year of publication
2001
Pages
109 - 118
Database
ISI
SICI code
0165-5728(20010201)113:1<109:LDCPCM>2.0.ZU;2-Y
Abstract
A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-alpha deficient (LT-alpha (-/-)) m ice compared to LT-alpha (+/+) mice when immunized with acetylcholine recep tor. However, only a partial prevention of clinical EAMG incidence was obse rved in LT-beta (-/-) mice compared to LT-beta (-/-) mice. LT-alpha (-/-) a nd LT-beta (-/-) mice had lower mean titers of total IgG, IgG(1), IgG(2a) a nd IgG(2b) and higher or equal mean titers of IgM anti AChR antibodies comp ared to controls. Therefore. LT-alpha (-/-) and LT-beta (-/-) AChR immunize d mice are capable of mounting a primary (IgM) humoral immune response to A ChR, but are less capable of switching to the pathogenic anti-AChR IgG isot ypes. LT could play a significant role in the pathogenesis of myasthenia gr avis. (C) 2001 Elsevier Science B.V. All rights reserved.