Resistance to experimental autoimmune myasthenia gravis in IL-6-deficient mice is associated with reduced germinal center formation and C3 production

Caishu Deng, Elzbieta Goluszko, Erdem Tüzün, Huan Yang, Premkumar Christadoss

Research output: Contribution to journalArticlepeer-review

87 Scopus citations

Abstract

To provide direct genetic evidence for a role of IL-6 in experimental autoimmune myasthenia gravis (EAMG), IL-6 gene KO (IL-6-/-) mice in the C57BL/6 background were immunized with Torpedo californica acetylcholine receptor (AChR) and evaluated for EAMG. Only 25% of AChR-immunized IL-6-/- mice developed clinical EAMG compared to 83% of C57BL/6 (wild-type) mice. A significant reduction in the secondary anti-AChR Ab of IgG, IgG2b, and IgG2c, but not the primary or secondary IgM response was observed in AChR-immunized IL-6-/- mice, suggesting a possible defect in T cell help and class switching to anti-AChR IgG2 isotype. The AChR-specific lymphocyte proliferative response, IFN-γ, and IL-10 production were suppressed in AChR-immunized IL-6-/- mice. EAMG resistance in IL-6-/- mice was associated with a significant reduction in germinal center formation and decreased serum complement C3 levels. The data provide the first direct genetic evidence for a key role of IL-6 in the autoimmune response to AChR and in EAMG pathogenesis.

Original languageEnglish (US)
Pages (from-to)1077-1083
Number of pages7
JournalJournal of Immunology
Volume169
Issue number2
DOIs
StatePublished - Jul 15 2002

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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