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Previous models distinguish training and priming based upon whether immune activation returns to baseline prior to secondary challenge. Tolerance is a protective mechanism whereby potent stimuli induce refractoriness to secondary challenge. Training and priming are important for innate memory responses that protect against infection, efficacy of vaccines, and maintaining innate immune cells in a state of readiness; tolerance prevents toxicity from excessive immune activation. Dysregulation of these processes can contribute to pathogenesis of autoimmune\/inflammatory conditions, post\u2010COVID\u201019 hyperinflammatory states, or sepsis\u2010associated immunoparalysis. Training, priming, and tolerance regulate similar \u201csignature\u201d inflammatory genes such as <jats:italic>TNF<\/jats:italic>, <jats:italic>IL6<\/jats:italic>, and <jats:italic>IL1B<\/jats:italic> and utilize overlapping epigenetic mechanisms. We review how interferons (IFNs), best known for activating JAK\u2013STAT signaling and interferon\u2010stimulated genes, also play a key role in regulating training, priming, and tolerance via chromatin\u2010mediated mechanisms. We present new data on how monocyte\u2010to\u2010macrophage differentiation modulates IFN\u2010\u03b3\u2010mediated priming, affects regulation of AP\u20101 and CEBP activity, and attenuates superinduction of inflammatory genes. We present a \u201ctraining\u2010priming continuum\u201d model that integrates IFN\u2010mediated priming into current concepts about training and tolerance and proposes a central role for STAT1 and IRF1.<\/jats:p>","DOI":"10.1111\/imr.13330","type":"journal-article","created":{"date-parts":[[2024,4,3]],"date-time":"2024-04-03T11:57:30Z","timestamp":1712145450000},"page":"257-275","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":50,"title":["Interferons and epigenetic mechanisms in training, priming and tolerance of monocytes and hematopoietic progenitors"],"prefix":"10.1111","volume":"323","author":[{"given":"Bikash","family":"Mishra","sequence":"first","affiliation":[{"name":"HSS Research Institute and David Z. Rosensweig Genomics Research Center Hospital for Special Surgery  New York New York USA"},{"name":"Immunology and Microbial Pathogenesis Program Weill Cornell Medicine  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9951-0646","authenticated-orcid":false,"given":"Lionel B.","family":"Ivashkiv","sequence":"additional","affiliation":[{"name":"HSS Research Institute and David Z. 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