Oak Jean S, Fruman David A
Department of Molecular Biology and Biochemistry, Center for Immunology, University of California, Irvine, CA 92697, USA.
Autoimmunity. 2007 Sep;40(6):433-41. doi: 10.1080/08916930701464780.
Activation of the phosphoinositide 3-kinase (PI3K) pathway promotes proliferation and survival in many different cell types of the immune system. PI3K acts downstream of receptors that mediate proliferation and survival in T cells, and required roles for individual class I PI3K catalytic isoforms have been established. Interestingly, mice with either augmented or diminished PI3K activity in T cells develop lymphoproliferation and signs of autoimmunity. Here, we summarize our current knowledge of mouse strains with hyperactive or reduced PI3K, different isoforms of class I PI3K in T cell-mediated immunity and autoimmunity, and the therapeutic implications for modulating this pathway for treatment of various autoimmune diseases.
磷酸肌醇3激酶(PI3K)信号通路的激活可促进免疫系统中多种不同细胞类型的增殖和存活。PI3K在介导T细胞增殖和存活的受体下游发挥作用,并且已确定了I类PI3K催化亚型的具体作用。有趣的是,T细胞中PI3K活性增强或减弱的小鼠均会出现淋巴细胞增殖和自身免疫迹象。在此,我们总结了目前关于PI3K活性过高或降低的小鼠品系、I类PI3K在T细胞介导的免疫和自身免疫中的不同亚型,以及调节该信号通路对治疗各种自身免疫性疾病的治疗意义的认识。