**6. Further mechanisms of angiotensin II-induced inflammation: human T and natural killer cells**

Co-stimulatory effects of angiotensinogen, AT I, and AT II on the proliferation of T and NK cells have been revealed [27]. T and NK cells were considered to have RAS elements, and they have been synthesizing AT II at the sites of inflammation creating a potential inflammatory amplification system [27, 28]. Th1 immune response has been disclosed to be crucial in the pathogenesis of inflammatory vascular diseases [28].

However, the interaction of AT II with Th1/Th2 cytokines during the development of inflammation is considered debatable. Recent studies have demonstrated the presence of RAS elements in human T and NK cells that they were capable to synthesize their own AT II [29]. Renin-induced inflammation has been related to the binding of AT II to the renin receptor in T cells, NK cells, and DC [29]. AT 2R which was previously considered to antagonize the actions of the AT1R and having beneficial effects in hypertension, cell growth, vascular remodeling, proliferation, and inflammation, currently, it has been thought to orchestrate the collective recruitment of leukocyte subsets to the sites of inflammation through mediating the effect of AT II [29, 30].
