Inhibitory effect of somatostatin on human T lymphocytes proliferation |
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| Institution: | 1. Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China;2. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China;3. Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI 48109, USA;4. Department of Pathology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China;5. Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA;1. Department of Engineering Structure and Mechanics, Wuhan University of Technology, Wuhan 430070, China;2. Department of Modern Mechanics, University of Science and Technology of China, Hefei 230027, China |
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| Abstract: | Somatostatin (SOM) was originally described as a growth hormone release inhibiting factor, but SOM and its specific receptors (SOM-r) have been shown to be expressed on both normal and activated T and B lymphocytes and other immunocompetent cells. In the present study we have demonstrated that SOM strongly inhibits the proliferation of human T lymphocytes when stimulated by PHA, Con A or alloantigens. However, SOM was most effective when the T cells were stimulated by an alloantigen rather than a polyclonal activator such as PHA and ConA. Moreover, SOM strongly inhibited the expression of activation markers such as CD69 and CD25 that are expressed on T lymphocytes during alloantigen stimulation. SOM also inhibited both CD28 and CD2 mediated T cell proliferation. Whereas proliferation of T cells induced by the engagement of CD3 antigen using specific mAbs was only marginally affected. Our results would support the concept that in humans SOM plays a key role in the modulation of T cell activation by interfering with the antigen-independent pathways CD2 and CD28. |
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