Imbalance between regulatory and effector T lymphocytes contributes to loss of immunotolerance and plays a permissive role in the initiation, perpetuation, and progression of chronic inflammatory diseases and autoimmune disorders. Regulatory/effector cell balance is governed by the CD39 ectonucleotidase, the prototype member of the NTPDase family that hydrolyzes ATP and ADP into AMP, subsequently converted into adenosine by CD73. Generation of adenosine impacts T-cell function as it contributes to the mechanism of suppression of Tregs and confers regulatory properties to pathogenic Th17-cells. CD39 cell distribution, mechanism of regulation and impact on inflammatory and regulatory signaling pathways are also discussed here. Innovative therapeutic strategies to boost CD39 levels and activity by either administering soluble ADPases or interfering with CD39 inhibitory signals are reviewed. Restoration of CD39 levels and function has enormous translational and clinical implications and should be regarded as an additional form of treatment to be deployed in the chronic inflammatory setting. The key role of CD39 in immunoregulation in the context of Crohn's disease, one of the most frequent manifestations of inflammatory bowel disease, and autoimmune hepatitis, an autoimmune disorder of the liver, is reviewed and discussed here.

调节性和效应性T淋巴细胞之间的失衡导致免疫耐受性丧失，并在慢性炎性疾病和自身免疫性疾病的发生，发展和发展中起着宽松的作用。调节/效应细胞的平衡由CD39胞外核苷酸酶控制，该酶是NTPDase家族的原型成员，该酶将ATP和ADP水解为AMP，随后被CD73转化为腺苷。腺苷的产生影响T细胞功能，因为它有助于抑制Treg的机制，并赋予致病性Th17细胞调节特性。CD39细胞分布，调节机制以及对炎症和调节信号通路的影响也在这里讨论。综述了通过施用可溶性ADPases或干扰CD39抑制信号来提高CD39水平和活性的创新治疗策略。CD39水平和功能的恢复具有巨大的翻译和临床意义，应被视为在慢性炎症环境中部署的另一种治疗形式。本文对CD39在克罗恩氏病（炎性肠病最常见的表现之一）和自身免疫性肝炎（一种肝脏自身免疫性疾病）的背景下在免疫调节中的关键作用进行了综述。