Hypoxia-associated　radioresistance　in　rectal　cancer　(RC)　has　severely　hampered　the　response　to　radioimmunotherapy　(iRT),　necessitating　innovative　strategies　to　enhance　RC　radiosensitivity　and　improve　iRT　efficacy.　Here,　a　catalytic　radiosensitizer,　DMPtNPS,　and　a　STING　agonist,　cGAMP,　are　integrated　to　overcome　RC　radioresistance　and　enhance　iRT.　DMPtNPS　promotes　efficient　X-ray　energy　transfer　to　generate　reactive　oxygen　species,　while　alleviating　hypoxia　within　tumors,　thereby　increasing　radiosensitivity.　Mechanistically,　the　transcriptomic　and　immunoassay　analysis　reveal　that　the　combination　of　DMPtNPS　and　RT　provokes　bidirectional　regulatory　effects　on　the　immune　response,　which　may　potentially　reduce　the　antitumor　efficacy.　To　mitigate　this,　cGAMP　is　loaded　into　DMPtNPS　to　reverse　the　negative　impact　of　DMPtNPS　and　RT　on　the　tumor　immune　microenvironment　(TiME)　through　the　type　I　interferon-dependent　pathway,　which　promotes　cancer　immunotherapy.　In　a　bilateral　tumor　model,　the　combination　treatment　of　RT,　DMPtNPS@cGAMP,　and　alpha　PD-1　demonstrates　a　durable　complete　response　at　the　primary　site　and　enhanced　abscopal　effect　at　the　distant　site.　This　study　highlights　the　critical　role　of　incorporating　catalytic　radiosensitizers　and　STING　agonists　into　the　iRT　approach　for　RC.　DMPtNPS　and　radiotherapy　(RT)　have　a　potential　to　decrease　tumor　hypoxia　and　enhance　radiosensitivity　while　provoking　bidirectional　regulatory　effects　on　the　immune　response.　Loading　cGAMP　on　DMPtNPS　reverse　the　negative　impact　on　the　immune　response　and　improves　immunotherapy　through　type　1　interferon　pathway.　When　combined　with　DMPtNPS@cGAMP,　RT　and　alpha　PD-1　therapy,　the　result　is　long-lasting　complete　response　and　improved　abscopal　effects.image