Infant nutrition is rich in lipids, and the adipose tissue has been adapted to properly break down neutral lipids and oxidize fatty acids in infancy. Accordingly, infant adipose tissue contains so-called beige adipocytes, which burn off lipids to heat, and impede fat storage and obesity. We show here that infant adipocytes are immune privileged sites for mitochondria due to a blockade in interferon regulatory factor 7 (IRF7)-signaling, which allows mitochondrial RNA to trigger beige adipocyte differentiation through mitochondria-to-nucleus signaling. These mechanisms serve to maintain an extensive mitochondrial network in beige adipocytes and protect against obesity. By contrast, fat storing white adipocytes lack these mechanisms and respond to their mitochondrial content with inflammation. We show that obesity subverts the immune privilege for mitochondria in adipocytes, which reduces mitochondrial mass and abrogates beige adipocyte development. In turn, suppressing IRF7 signaling and restoring the RNA-mediated mitochondria-to-nucleus signaling in adipocytes effectively reduces obesity.