**8. Conclusions**

Hyperactivity of the RAS resulting elevated AT II might contribute to all stages of inflammatory responses including ocular inflammation. ACE2 is more likely to establish a protective axis of RAS involving ACE2/Ang-(1–7)/Mas, which counteract the proinflammatory and hypertrophic effects of the ACE/AngII/AT1R axis. AT II might have also co-stimulatory effects on T cells, NK cells, and DC, which have specific elements of the RAS. RAS antagonists might be used in conjunction with other anti-inflammatory agents as therapy for common diseases in which inflammation plays a major pathogenic role.
