In a recent study, we demonstrated that bacteria-specific Th1 (IFN-γ producing CD4 T cells) and Th17 (IL-17 producing CD4 T cells) cells played pivotal roles in restraining Hi infection [12]; thus, we first examined Th1 and Th17 responses induced by Hi in the lupus-prone mice. The gene discussed is CD4; the disease is systemic lupus erythematosus.