Ledesma Edgar, Martínez Ignacio, Córdova Yolanda, Rodríguez-Sosa Miriam, Monroy Alberto, Mora Lourdes, Soto Isabel, Ramos Gerardo, Weiss Benny, Santiago Osorio Edelmiro
Laboratorio de Biología Celular y Molecular del Cáncer, UIDCC, FES-Zaragoza, UNAM, Mexico.
Cytokine. 2004 Apr 21;26(2):66-72. doi: 10.1016/j.cyto.2003.12.009.
Interleukin-1 alpha (IL-1alpha) and beta (IL-1beta) are well known factors that stimulate hematopoiesis, nevertheless there are reports that show that they can also inhibit this activity. While both IL-1alpha and IL-1beta induce the expression of hematopoietic cytokines, such as growth factors and their receptors on myeloid cells, helping thus to regulate hematopoiesis, it is not known if their inhibitory activity is also mediated through the induction of other specific cytokines. In this work we show that recombinant human IL-1beta (rhIL-1beta) inhibits the proliferation of a mouse IL-3-dependent myeloid multipotent cell line (32D cl3), without inducing its differentiation. We show that rhIL-1beta induces in 32D cl3 cells the expression of the tumor necrosis factor alpha (TNF-alpha) gene, a well known growth inhibitor, and that the rhIL-1beta growth inhibition property on 32D cl3 cells is partially due to this secreted TNF-alpha, hinting thus that the inhibition of hematopoiesis by IL-1 is mediated through other induced cytokines.
白细胞介素-1α（IL-1α）和β（IL-1β）是刺激造血的知名因子，然而有报道表明它们也可抑制这种活性。虽然IL-1α和IL-1β都能诱导造血细胞因子的表达，如髓系细胞上的生长因子及其受体，从而有助于调节造血，但尚不清楚它们的抑制活性是否也通过诱导其他特定细胞因子介导。在这项研究中，我们表明重组人IL-1β（rhIL-1β）可抑制小鼠IL-3依赖的髓系多能细胞系（32D cl3）的增殖，且不诱导其分化。我们发现rhIL-1β可诱导32D cl3细胞中肿瘤坏死因子α（TNF-α）基因的表达，TNF-α是一种众所周知的生长抑制剂，并且rhIL-1β对32D cl3细胞的生长抑制特性部分归因于这种分泌的TNF-α，因此提示IL-1对造血的抑制是通过其他诱导的细胞因子介导的。
