Introduction: In this study, we describe establishment and characterization of stable Ba/F3 cell lines transfected with the two isoforms of the human IL-11Rα receptor (α1 full length or α2 lacking the intracytoplasmic domain) in combination with human gp130. We used these cells lines to evaluate the contribution of the intracytoplasmic domain of IL-11Rα in ligand binding and signal transduction.Materials and Methods: Ba/F3 transfected cells were established by electroporating pLXSP/IL-11Rα1 or pLXSP/IL-11Rα2 and pRCNeo/gp130. Receptors expression was controlled by Western blot and flow cytometry analyses. Proliferation assays: transfected Ba/F3 cells were additioned with serial dilutions either of IL-11, of IL-6 in the presence or not of sIL-6Rα or a mixture of anti-human gp130 mAbs (B-P8 and B-S12). In a second type of assay, cells were additioned with IL-11 or IL-6 plus sIL-6Rα, and serial dilutions of anti-human IL-6Rα mAbs (PM1, B-N12) or anti-human gp130 mAbs (B-R3, B-P4). Cellular proliferation was assessed by a MTT based assay.Results: IL-11Rα1 and IL-11Rα2 were each expressed as three bands, with MW in agreement with that of the polypeptide backbone (47 and 44 kDa respectively) with no, one or two N-linked sugars. Ba/F3 cells co-transfected with IL-11Rα1 and gp130 (B13Rα1) or IL-11Rα2 and gp130 (B13Rα2) bound IL-11-thioredoxin with similar efficiencies and proliferated with superimposable dose-response curves to IL-11, demonstrating that the intracellular domain of IL-11Rα has no significant contribution on ligand binding and signaling. B-P8 and B-S12 mAbs displayed agonistic and synergistic activity of the two IL-11R transfectants induced either by IL-11 or the combination of IL-6 plus sIL-6Rα; B-R3 and B-P4 inhibited proliferation of these cells induced either by IL-11 or the combination of IL-6 plus sIL-6Rα.Conclusion: Our results demonstrate that the intracellular domain of IL-11Rα has no significant contribution on ligand binding and signaling. Analysis of a set of anti-human gp130 mAbs confirms the similar responsiveness of B13Rα1 and B13Rα2 transfectants.