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Moreover, it was established that CRP exacerbates acute kidney injury in mice, and this was associated with the heightened renal accumulation of myeloid-derived cells with suppressor functions, with a research study revealing CRPs ability to expand and trigger the increased FcRIIb-independent production of iROS in these cells, as well as its ability to FcRIIb-dependently enhance the T cell-suppressive action [154]
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