The mechanisms by which the Th17 immune response would favor the development of anti-tRNA-ILD are diverse; it has been recognized that the synergistic activity between IL-6 and TGF-β induces the transformation of regulatory T-lymphocytes (Treg) into Th17-lymphocytes, thus reducing the number of cells competent of counteracting the activity of self-reactive T- [31] and B-lymphocytes [32]. The gene discussed is IL6; the disease is interstitial lung disease.