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While these responses can be beneficial in host defense, aberrant activation of inflammatory, lytic cell death pathways can be pathogenic. Emerging evidence suggests that cellular metabolic disruption can promote inflammatory cell death, but the mechanistic connections between these processes are not well understood, limiting our ability to identify regulatory nodes that can be therapeutically targeted. Here, we found that intracellular levels of the metabolic cofactor nicotinamide adenine dinucleotide (NAD+) were depleted in response to cell death triggers that drive pyroptosis, necroptosis, PANoptosis, and ferroptosis. However, restoring NAD+ inhibited PANoptosis but not the other forms of cell death. Mechanistically, NAD+ restoration reduced the expression of PANoptotic sensors or regulators, including the transcription factor IRF1, a critical factor for innate immune sensor priming in PANoptosis. Our findings thereby suggest that NAD+ depletion is an early cell death signaling event and that restoring NAD+ levels specifically blocks PANoptosis by suppressing priming. Hence, targeting NAD+ metabolism represents a potential therapeutic strategy for infectious and inflammatory diseases associated with dysregulated PANoptosis.<\/jats:p>","DOI":"10.1093\/jimmun\/vkag203","type":"journal-article","created":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T12:57:10Z","timestamp":1785157030000},"source":"Crossref","is-referenced-by-count":1,"title":["NAD+ depletion links metabolic stress to drive innate immune priming and selectively control PANoptosis"],"prefix":"10.1093","volume":"215","author":[{"given":"Roman","family":"Sarkar","sequence":"first","affiliation":[{"name":"Department of Immunology, St. Jude Children\u2019s Research Hospital , Memphis, TN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nagakannan","family":"Pandian","sequence":"additional","affiliation":[{"name":"Department of Immunology, St. Jude Children\u2019s Research Hospital , Memphis, TN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Balamurugan","family":"Sundaram","sequence":"additional","affiliation":[{"name":"Department of Immunology, St. Jude Children\u2019s Research Hospital , Memphis, TN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bhesh Raj","family":"Sharma","sequence":"additional","affiliation":[{"name":"Department of Immunology, St. Jude Children\u2019s Research Hospital , Memphis, TN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter A","family":"Gorsuch","sequence":"additional","affiliation":[{"name":"Department of Immunology, St. Jude Children\u2019s Research Hospital , Memphis, TN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rebecca E","family":"Tweedell","sequence":"additional","affiliation":[{"name":"Department of Immunology, St. Jude Children\u2019s Research Hospital , Memphis, TN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6395-6443","authenticated-orcid":false,"given":"Thirumala-Devi","family":"Kanneganti","sequence":"additional","affiliation":[{"name":"Department of Immunology, St. Jude Children\u2019s Research Hospital , Memphis, TN,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2026,7,27]]},"reference":[{"key":"2026090710440471200_vkag203-B1","doi-asserted-by":"publisher","first-page":"e2250235","DOI":"10.1002\/eji.202250235","article-title":"Innate immune inflammatory cell death: PANoptosis and PANoptosomes in host defense and disease","volume":"53","author":"Chen","year":"2023","journal-title":"Eur J Immunol"},{"key":"2026090710440471200_vkag203-B2","doi-asserted-by":"publisher","first-page":"1106","DOI":"10.1038\/s41423-020-00630-3","article-title":"Necroptosis, pyroptosis and apoptosis: 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