IL-17-producing T_h (T_h17) comprise a distinct lineage of pro-inflammatory T_h that are major contributors to autoimmune diseases. Treatment with IL-6 and transforming growth factor β (TGFβ) induces naive CD4⁺ T cells to generate T_h17, which also requires expression of the IL-6/TGFβ target RORγt. We reported that IL-6 transduces two signaling pathways via tyrosine redidues of the signal transducer gp130: one depends on signal transducers and activators of transcription (STAT)-3 activation and the other on Src homology region 2 domain-containing phosphatase 2 (SHP2)/Grb2 associated binder (Gab)/mitogen-activated protein kinase (MAPK) activation. Here, we showed that CD4⁺ T cells carrying a mutant gp130 that transduces the SHP2/Gab/MAPK pathway but not the STAT3-mediated one failed to develop into T_h17, while CD4⁺ T cells whose mutant gp130 transduces the STAT3 signal only generated T_h17, indicating that IL-6 acts directly on T cells through the tyrosine residues of gp130 required for STAT3 activation to promote the development of T_h17. Moreover, we found that gp130–STAT3 pathway is essential for T_h17 development and for the expression of RORγt by using T cells specifically lacking gp130 and STAT3. Noteworthy is that the regulatory T cell (Treg) percentages and numbers were comparable between all mutant mice we tested in vivo, although we showed that IL-6–gp130–STAT3 pathway suppressed Treg development in vitro. Thus, we conclude that IL-6 acts directly to promote the development of T_h17 by activating the T cell gp130–STAT3 pathway but has a minimum effect on Treg development at least in the steady state in vivo. Therefore, blockade of IL-6–gp130–STAT3 pathway in CD4⁺ T cells could be a good target for controlling unwanted T_h17-mediated immune responses including autoimmune diseases.