Recall immune memory: A new tool for generating late onset autoimmune myasthenia gravis

Sue Stacy, Anthony J. Infante, Katherine A. Wall, Keith Krolick, Ellen Kraig

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

Most patients with autoimmune myasthenia gravis (MG) produce autoantibodies against their muscle acetylcholine receptors (AChR), causing debilitating muscle weakness. Approximately 60% of MG patients first exhibit myasthenic symptoms after the age of 40. Yet, in the C57BL/6 mouse model of MG, older mice are resistant to induction of myasthenia gravis. To understand the immunological basis for this resistance, the effects of age on the B-cell responses to AChR from Torpedo californica, the inducing antigen, were addressed. As expected, the primary B-cell response was lower in 20-month-old mice than in 2-month-old mice; the isotype profile was not altered by age. When mice were re-immunized, the anti-T-AChR titers increased in both young and old animals, suggesting that a memory response was elicited. Importantly, memory B-cells activated in young animals were largely resistant to the age-associated loss of immune function and the recall memory response was vigorous. Furthermore, the antibodies produced in re-stimulated older mice were functional, as evidenced by the appearance of MG symptoms in some of these animals. Thus, by eliciting a recall memory response, the first examples of late onset MG in mice have been generated. By analogy, late onset MG in humans may be due to re-activation of B-cell responses initiated at a younger age.

Original languageEnglish (US)
Pages (from-to)931-940
Number of pages10
JournalMechanisms of Ageing and Development
Volume124
Issue number8-9
DOIs
StatePublished - Jan 1 2003

Keywords

  • Autoimmunity
  • B lymphocytes
  • Immunological memory

ASJC Scopus subject areas

  • Aging
  • Developmental Biology

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