TLR3 and myasthenia gravis: A close link between AChR expression and autosensitization in the inflamed hyperplastic MG thymic milieu has been postulated, since pro-inflammatory and Toll-like receptor (i.e., TLR3) stimuli are able to increase the AChR-α subunit expression in TECs in vitro, and to induce thymic hyperplastic changes and anti-AChR autoantibody production in vivo [38].