{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T13:01:34Z","timestamp":1792587694832,"version":"4.5.0"},"reference-count":46,"publisher":"American Society of Hematology","issue":"8","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,8,21]]},"abstract":"<jats:sec>\n                  <jats:title>Abstract<\/jats:title>\n                  <jats:p>Anemia of inflammation (AI) is the second most common form of anemia and is prevalent in patients with chronic inflammatory states, such as infection, autoimmunity, and cancer. Interleukin 6 (IL-6) is well-known to induce the iron-sequestering hormone hepcidin, which results in iron-restricted anemia. The contributions of other proinflammatory cytokines, such as tumor necrosis factor-\u03b1 (TNF\u03b1) and interferon gamma (IFN\u03b3), are less understood in the pathophysiology of AI. This study investigated the role of TNF\u03b1 in a mouse model of AI by administering heat-killed Brucella abortus (HKBA) to germ line TNF\u03b1 knockout (KO) mice. We hypothesized that TNF\u03b1 possessed an important role in restoring steady-state erythropoiesis after inflammatory insult. TNF\u03b1KO injected with HKBA displayed a chronic anemia, with elevated proinflammatory IL12p40 and IFN\u03b3 cytokines that did not resolve. However, IFN\u03b3KO and TNF\u03b1KO\/FN\u03b3KO double knockout mice showed reduced inflammation and anemia following HKBA administration. Because IFN\u03b3KO displayed normal serum TNF\u03b1 and IL12p40 levels, we hypothesized that the persistent anemia was IFN\u03b3 induced and TNF\u03b1 was necessary for AI cessation. However, treatment with recombinant TNF\u03b1 (rTNF\u03b1) accelerated death, while reducing IFN\u03b3 using an anti-IFN\u03b3 antibody (Ab) only briefly improved anemia. Only the combination of both the Ab and rTNF\u03b1 together reversed the hyperinflammatory phenotype, restored erythropoiesis, and prevented death of TNF\u03b1KO + HKBA mice. Our data provide compelling evidence for an anti-inflammatory role of TNF\u03b1 that is necessary for the restoration of erythropoiesis and mitigation of proinflammatory IFN\u03b3 action in a mouse model of AI.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1182\/blood.2025029352","type":"journal-article","created":{"date-parts":[[2025,6,13]],"date-time":"2025-06-13T11:04:33Z","timestamp":1749812673000},"page":"984-997","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":4,"title":["TNF\u03b1 signaling restores steady-state hematopoiesis in a TNF\u03b1KO mouse model of anemia of inflammation"],"prefix":"10.1182","volume":"146","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6602-1854","authenticated-orcid":false,"given":"Amaliris","family":"Guerra","sequence":"first","affiliation":[{"name":"1Division of Hematology, Department of Pediatrics, The Children\u2019s Hospital of Philadelphia, Philadelphia, 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