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Tumor necrosis factor alpha-induced protein 8-like 2 (TIPE2) is a member of the TNFAIP8 family, preferentially expressed in myeloid cell types and acting as a critical regulator of immunity and metabolism. TIPE2 inhibits immune cell activation and inflammatory gene expression, constraining both innate and adaptive immune responses to maintain immune homeostasis. Mechanistically, TIPE2 modulates cellular lipid metabolism, autophagy (via TAK1/JNK pathway inhibition), and mitochondrial respiration. Its expression is dynamically regulated in disease states, such as being suppressed in acute inflammation and induced in metabolic syndrome. Because of its dual regulatory function, TIPE2 serves as an immune “brake,” and is a promising novel therapeutic target for cardiovascular disease, cancer, and inflammatory conditions
null (as of 2025, direct drugs are not available; mechanism for potential therapeutics would be immune and metabolic checkpoint modulation via inhibition or enhancement of TIPE2’s activity)
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