Evidence show that Th1 and Th2 become resistant to proliferation

Evidence show that Th1 and Th2 become resistant to proliferation towards Th17 and its IL23 is stimulated by IL-17 cytokine. The early defining phase of Th17 differentiation from naïve CD4 cell is induced by an anti-inflammatory cytokine called TGF beta and IL-6. The presence of these cytokines plays a role in differentiation of Th17. TGF beta is also known to play a role in differentiation of T regulatory cells. Therefore, depending on the presence of IL-6, TGF beta either induces the differentiation of T reg. cell or Th17 from naïve CD4 T cells. The presence of TGF beta and IL-6 up-regulate the expression of IL 23 receptor on developing Th17 cells, which causes rapid proliferation of these cells after interacting with IL-23. This is known to play an important role in further survival, expansion, and programming of Th17 cells (Ivanov, & Lindén 280). TGF beta and IL-6 induce expression of orphan nuclear receptor RORgammat that is considered the main transcription factor of differentiation of Th17. Th17 cells regulate the recruitment of inflammatory cells such as neutrophils to the site of infection and attack the pathogen by secreting defence. This causes a degree of inflammation and removal of phagocyte from the site of infection. Because of its inflammatory effects, Th17 is also thought to act as an effector of autoimmune disorders such as ulcerative colitis.