Auto-reactive T cells are kept tolerant in the body by multiple mechanisms. How they are activated and precipitate tissue specific autoimmunity; especially the cytokine(s) that support their survival, expansion and attack on self-tissues is not fully understood. To explore this question, we established a simplified model system. A transfer of fully differentiated, pure T-helper17 (Th17) cells with skin-reactive TCR (Th17 DSG3 H1 TCR Tg) into sub-lethally irradiated recipients, reproducibly caused severe autoimmune dermatitis. Intriguingly, the expansion of transferred auto-reactive Th17 and the penetrance of dermatitis in this model was abrogated by treating the recipients by cocktail of antibiotics which is known to deplete wide spectrum of commensal microbiota. To understand how microbiota helps expansion of self-reactive Th17, we compared homeostatic cytokines important for T cell homeostasis (IL-7, TSLP, IL-15, TGFβ) from various organs before and after antibiotics treatment. Our data indicated that production of these cytokines from organs are stable at homeostaic condition, but drastically change after antibiotic treatement, which influences expansion and survival of the fully differentiated autoreactive Th17. Thus, commensal microbiota interacts with, and stimulates cytokine expression from organs that support systemic T cells response, which can result in autoimmune symptoms.