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Disequilibrium of T helper type 1, 2 and 17 cells and regulatory T cells during the development of experimental autoimmune myasthenia gravis
Author(s) -
Mu Lili,
Sun Bo,
Kong Qingfei,
Wang Jinghua,
Wang Guangyou,
Zhang Shujuan,
Wang Dandan,
Liu Yumei,
Liu Yixi,
An Huixia,
Li Hulun
Publication year - 2009
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2009.03089.x
Subject(s) - myasthenia gravis , immunology , acetylcholine receptor , autoimmune disease , cytokine , biology , antibody , receptor , medicine
Summary 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.