Role of Beclin-1 for the induction of autophagy in B lymphocytes

点击翻译按钮获取中文摘要

Autophagy is a catabolic process during which portions of the cytoplasm are sequestered by double-membraned vesicles and delivered to lysosomes. During the past decade the molecular understanding of this degradative process has been promoted enormously, and currently the role of autophagy in pathogenic events including cancer, neurodegeneration, or infectious diseases is deciphered. B lymphocytes are a central component of adaptive immunity, and the production of soluble immunoglobulins represents the main effector function of B lymphocytes which have been differentiated to plasma cells. In B lymphocytes, autophagy plays an important role during both development and MHC class II-dependent antigen presentation. It seems that in B lymphocytes, autophagy is induced specifically by apoptotic B cell antigen receptor signaling. Generally, one initial step during the induction of autophagy is the activation of PI3K class III. This activation in turn depends on a multi-protein complex including Beclin-1/Atg6. The aim of the described project is to analyze the role of Beclin-1 during the induction of autophagy in B lymphocytes. The findings should then lead to a better understanding of the mechanisms regulating B cell homeostasis and thereby critically influencing the humoral immune response.