The immuno-metabolite itaconate, generated by the enzyme ACOD1 in macrophages, plays a critical role in regulating immune cell signaling and metabolism. ACOD1 is induced by various stimuli, including microbial pathogen-associated molecular patterns (PAMPs), cytokines, and type I interferons. Itaconate exerts anti-microbial and immunomodulatory effects by inhibiting key enzymes such as succinate dehydrogenase (SDH) and Tet2, and by modifying signaling proteins through post-translational modifications (PTMs), particularly at cysteine residues. These modifications affect pathways involved in inflammation, immune cell activation, and metabolic reprogramming. Itaconate modulates the function of immune cells, including macrophages and neutrophils, by inhibiting the production of pro-inflammatory cytokines and reducing oxidative stress. It also influences the activity of signaling proteins such as STING, SYK, JAK1, and KEAP1, as well as transcription factors like TFEB and Tet2. These effects contribute to the regulation of immune responses and the control of inflammation. In addition to macrophages, neutrophils also produce itaconate, and its presence can influence neutrophil function and the resolution of inflammation. The metabolite can act on other cell types, including T cells and antigen-presenting cells, through paracrine or systemic mechanisms. It has been shown to enhance adaptive immune responses by promoting the generation of protective T cell immunity and by modulating the function of dendritic cells. Itaconate also plays a role in the regulation of adaptive immune responses, including the differentiation of T helper cells and the suppression of T cell activation. It has been shown to inhibit Th17 differentiation and reduce the production of pro-inflammatory cytokines. Furthermore, itaconate can influence the function of tumor-associated macrophages, which can suppress T cell anti-tumor immune responses. The study of itaconate has revealed its potential as a therapeutic target for the treatment of inflammatory and infectious diseases. It has been shown to reduce the severity of autoimmune diseases such as systemic lupus erythematosus (SLE) by inhibiting the production of type I interferons and reducing systemic inflammation. Overall, itaconate serves as a key regulator of immune cell signaling and metabolism, with implications for both innate and adaptive immune responses.The immuno-metabolite itaconate, generated by the enzyme ACOD1 in macrophages, plays a critical role in regulating immune cell signaling and metabolism. ACOD1 is induced by various stimuli, including microbial pathogen-associated molecular patterns (PAMPs), cytokines, and type I interferons. Itaconate exerts anti-microbial and immunomodulatory effects by inhibiting key enzymes such as succinate dehydrogenase (SDH) and Tet2, and by modifying signaling proteins through post-translational modifications (PTMs), particularly at cysteine residues. These modifications affect pathways involved in inflammation, immune cell activation, and metabolic reprogramming. Itaconate modulates the function of immune cells, including macrophages and neutrophils, by inhibiting the production of pro-inflammatory cytokines and reducing oxidative stress. It also influences the activity of signaling proteins such as STING, SYK, JAK1, and KEAP1, as well as transcription factors like TFEB and Tet2. These effects contribute to the regulation of immune responses and the control of inflammation. In addition to macrophages, neutrophils also produce itaconate, and its presence can influence neutrophil function and the resolution of inflammation. The metabolite can act on other cell types, including T cells and antigen-presenting cells, through paracrine or systemic mechanisms. It has been shown to enhance adaptive immune responses by promoting the generation of protective T cell immunity and by modulating the function of dendritic cells. Itaconate also plays a role in the regulation of adaptive immune responses, including the differentiation of T helper cells and the suppression of T cell activation. It has been shown to inhibit Th17 differentiation and reduce the production of pro-inflammatory cytokines. Furthermore, itaconate can influence the function of tumor-associated macrophages, which can suppress T cell anti-tumor immune responses. The study of itaconate has revealed its potential as a therapeutic target for the treatment of inflammatory and infectious diseases. It has been shown to reduce the severity of autoimmune diseases such as systemic lupus erythematosus (SLE) by inhibiting the production of type I interferons and reducing systemic inflammation. Overall, itaconate serves as a key regulator of immune cell signaling and metabolism, with implications for both innate and adaptive immune responses.