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Nitrated recombinant CCL2 is a post-translationally modified form of the chemokine C-C motif ligand 2 (CCL2) used in preclinical research to model tumor-induced immune evasion. In bladder cancer, the tumor microenvironment promotes the nitration of CCL2, which disrupts its normal function of recruiting tumor-protective CCR2+ T cells. Experimental nitration of recombinant CCL2 has been shown to abolish its therapeutic efficacy, leading instead to decreased T cell infiltration and increased recruitment of immunosuppressive monocytes. This modified protein serves as a critical tool for understanding how oxidative stress in the tumor microenvironment alters chemokine signaling and contributes to cancer progression.
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