Hershfield Michael S
Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
Eur J Immunol. 2005 Jan;35(1):25-30. doi: 10.1002/eji.200425738.
There is growing interest in manipulating adenosine (Ado) signal transduction to control inflammation and autoimmunity. This concept probably originated with the discovery of severe combined immunodeficiency disease (SCID) in infants with inherited deficiency of adenosine deaminase (ADA). However, the basis for immunosuppression by Ado has not been well defined, and effects of 2'-deoxyadenosine (dAdo), which does not activate Ado receptors, have also been implicated in causing SCID. Here I discuss recent evidence that Ado, acting through its A2A receptor, interferes with NF-kappa B activation in antigen-receptor-stimulated B and T lymphocytes. I also assess the relative contributions of Ado and dAdo to the pathogenesis of ADA-deficient SCID.
通过操纵腺苷（Ado）信号转导来控制炎症和自身免疫的兴趣日益浓厚。这一概念可能起源于发现患有腺苷脱氨酶（ADA）遗传性缺乏症的婴儿患有严重联合免疫缺陷病（SCID）。然而，Ado免疫抑制的基础尚未明确界定，且不激活Ado受体的2'-脱氧腺苷（dAdo）的作用也被认为与SCID的发生有关。在此，我讨论了最近的证据，即Ado通过其A2A受体发挥作用，干扰抗原受体刺激的B和T淋巴细胞中NF-κB的激活。我还评估了Ado和dAdo对ADA缺乏型SCID发病机制的相对贡献。
