Rich S A, Owens T R
J Interferon Res. 1984 Summer;4(3):335-45. doi: 10.1089/jir.1984.4.335.
Raji and Daudi are human B lymphoblastoid cell lines that readily form lupus inclusions (LIs; TRS) when grown in medium supplemented with leukocyte-, or fibroblast-derived interferon (IFN-alpha, -beta, respectively). WISH, MDBK, and GM2504 are three cell lines commonly used to measure antiviral activities. None of them form LIs in their antiviral response to alpha or immune (gamma)IFN. This distinguishes between the abilities of a cell to develop an antiviral state and to form LIs in response to IFN. Human (Hu) lymphoblastoid IFN and the two pure and homogeneous recombinant human IFN-alpha proteins IFLrA and IFLrD induce LIs in Raji cells and Daudi cells. In Daudi, a simultaneous inhibition of cell growth occurs. When compared by antiviral activities, IFLrA inhibits the growth of Daudi cells more, while IFLrD induces the greater frequency of LIs. According to molecular concentration, IFLrA and IFLrD at 133 X 10(-13) M induce LIs in Daudi cells to their maximum frequency. Growth inhibition for these same cell samples is also at maximum for IFLrA, but only 25% of maximum for IFLrD. Our results with Raji and Daudi cells provide evidence against a cause-and-effect relationship between these two biologic responses to IFN by Daudi cells. They also provide evidence for distinct, but interacting, intracellular pathways. This phenomenon is a new explanation for some of the biologic diversity shown for the HuIFNs-alpha.
拉吉细胞系和道迪细胞系是人类B淋巴母细胞系，当在添加了白细胞或成纤维细胞衍生的干扰素（分别为α干扰素、β干扰素）的培养基中生长时，它们很容易形成狼疮包涵体（LIs；TRS）。WISH、MDBK和GM2504是常用于测量抗病毒活性的三种细胞系。它们在对α干扰素或免疫（γ）干扰素的抗病毒反应中均不形成LIs。这区分了细胞产生抗病毒状态和对干扰素形成LIs的能力。人（Hu）淋巴母细胞干扰素以及两种纯的、同质的重组人α干扰素蛋白IFLrA和IFLrD可在拉吉细胞和道迪细胞中诱导形成LIs。在道迪细胞中，同时会出现细胞生长抑制。通过抗病毒活性比较，IFLrA对道迪细胞生长的抑制作用更强，而IFLrD诱导形成LIs的频率更高。根据分子浓度，133×10⁻¹³ M的IFLrA和IFLrD可使道迪细胞中LIs的诱导频率达到最高。对于这些相同的细胞样本，IFLrA的生长抑制作用也达到最大，但IFLrD的生长抑制作用仅为最大值的25%。我们对拉吉细胞系和道迪细胞系的研究结果提供了证据，反对道迪细胞对干扰素的这两种生物学反应之间存在因果关系。它们还为不同但相互作用的细胞内途径提供了证据。这种现象为HuIFNs-α所表现出的一些生物学多样性提供了新的解释。
