BackgroundIt has been well known that the surface antigen 1(SAG 1) of T.gondii plays an important role in the invasion of Tachyzoite into host cells. However whether it also play a role in the intracellular parasitism of T.gondii remains unclear. The main purpose of this study was to determine the effect of SAG1 on host cells and investigate the underlying mechanism. MethodsSAG1 was overexpressed in human embryonic kidney cell 293(HEK) by transfection. Autophagy was determined by fluorescent microscope and flow cytometry (FCM) in HEK293 cells co-transfected with Flag-SAG1 and EGFP-LC3. The interaction of SAG1 and RACK1 was measured by co-immunoprecipitation(Co-IP), GST pulldown and fluorescent microscope. The expression of cytokines including IL-1β, IL-6, and IL-12 was determined by qRT-PCR. The expression of LC3, Ki67 and RACK1 was detected by Western blot. Cellular senescence was measured by β-galactosidase staining.ResultsWe found that overexpression of SAG1 in human embryonic kidney cells (HEK293) induces non-canonical autophagy and inhibition of autophagy using hydroxychloroquine (HCQ) significantly decreases the cell viability of HEK293 cells. Mechanically, we identified RACK1, an intracellular multifunctional protein as a binding partner of SAG1. Depletion of RACK1 inhibited SAG1 induces non-autophagy and decreases the enhanced expression of cytokines including IL-1β, IL-6, IL-12 and TNF-α in SAG1 overexpressing cells. ConclusionThese data showed that SAG1 could induce non-canonical autophagy and facilitate the expression of IL-1β, IL-6, IL-12 and TNF-α by interacting with RACK1, maintaining the viability of host cells. Our results suggests a new contribution of SAG1 in the intracellular parasitism.