Genetic deficiency of estrogen receptor alpha fails to influence experimental autoimmune myasthenia gravis pathogenesis

J Neuroimmunol. 2011 May;234(1-2):165-7. doi: 10.1016/j.jneuroim.2011.03.002. Epub 2011 Apr 8.

Abstract

Autoimmune myasthenia gravis (MG) is characterized by T cell and antibody responses to muscle nicotinic acetylcholine receptor (AChR). It is well known that MG as other autoimmune diseases is more prevalent in women than men and estrogen administration enhances experimental autoimmune MG (EAMG) severity. To determine whether estrogen influences EAMG pathogenesis through estrogen receptor alpha (ERα) activation, ERα knockout (KO) and wild-type (WT) C57BL/6 mice were immunized with AChR. ERα KO mice were equally susceptible to EAMG as WT mice and exhibited comparable antibody and immunopathological responses to AChR, suggesting a lack of involvement of ERα in EAMG pathogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies / blood
  • Cytokines / metabolism
  • Disease Models, Animal
  • Enzyme-Linked Immunosorbent Assay / methods
  • Estrogen Receptor alpha / deficiency*
  • Genetic Predisposition to Disease / genetics
  • Hand Strength / physiology
  • Immunization / adverse effects
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myasthenia Gravis, Autoimmune, Experimental / genetics*
  • Myasthenia Gravis, Autoimmune, Experimental / immunology*
  • Myasthenia Gravis, Autoimmune, Experimental / pathology*
  • Myasthenia Gravis, Autoimmune, Experimental / physiopathology
  • Receptors, Cholinergic / immunology
  • Time Factors

Substances

  • Antibodies
  • Cytokines
  • Estrogen Receptor alpha
  • Receptors, Cholinergic