Abstract

Myasthenia gravis (MG) is an autoimmune disease that affects the transmission signals from nerves to muscles. The basic pathology is the production of anti-acetylcholine receptor (AChR) antibodies (AChRAb) which is the consequence for the generation of autoreactive T lymphocytes responsing to AChR. However, the molecular mechanism of MG and the production of autoreactive T lymphocytes remain elusive. Recently beside its pivotal role in reproduction, the pituitary hormone prolactin (PRL) has been attributed to an immunomodulatory function. Furthermore it has been shown to be expressed in T cells and conversely it also affects the function of T cells, such as directly stimulating the proliferation and survival of T lymphocytes. In addition, elevated PRL levels frequently are described in autoimmune diseases, such as systemic lupus erythematosus (SLE) and multiple sclerosis (MS). So we hypothesized that the stimulating effect of PRL on T-cells function may be implied in the pathogenesis of MG and, perhaps, prolactin may be a promising therapeutic target for MG.

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