Experimental autoimmune myasthenia gravis (EAMG), an animal model of myasthenia gravis (MG), is a rare organ-specific autoimmune disease targeting the autoantigen nicotinic acetylcholine receptor (AChR). We show here that the balance of T helper type 1 (Th1), Th2, Th17 and regulatory T (Treg) subsets of CD4(+) helper T cells were redistributed during the development of EAMG and that the interleukin-17 (IL-17) cytokine is involved in this disease. The ratio of Th17 cells changed most notably with disease progression accompanied by an up-regulated level of IL-17. Moreover, the proliferative ability of AChR peptide-specific T cells and the anti-AChR antibody-secreting cells increased when stimulated by IL-17 in vitro. These findings suggested that the disequilibrium of the CD4(+) helper T-cell subsets could promote the development of EAMG, and the pathogenic mechanism by which Th17 cells drives autoimmune responses by secreting cytokine IL-17 provides a new target for myasthenia gravis therapy.