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We report that the IRE1\u03b1-XBP1 branch of the unfolded protein response (UPR) inhibits IFN-\u03b1 production by TLR7- or TLR9-activated pDCs. In SSc patients, UPR gene expression was reduced in pDCs, which inversely correlated with IFN-I\u2013stimulated gene expression. CXCL4, a chemokine highly secreted in SSc patients, downregulated IRE1\u03b1-XBP1\u2013controlled genes and promoted IFN-\u03b1 production by pDCs. Mechanistically, IRE1\u03b1-XBP1 activation rewired glycolysis to serine biosynthesis by inducing phosphoglycerate dehydrogenase (PHGDH) expression. This process reduced pyruvate access to the tricarboxylic acid (TCA) cycle and blunted mitochondrial ATP generation, which are essential for pDC IFN-I responses. Notably, PHGDH expression was reduced in pDCs from patients with SSc and SLE, and pharmacological blockade of TCA cycle reactions inhibited IFN-I responses in pDCs from these patients. 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