{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T17:11:18Z","timestamp":1785431478510,"version":"3.56.0"},"posted":{"date-parts":[[2026,7,22]]},"group-title":"Immunology","reference-count":79,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T00:00:00Z","timestamp":1784678400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"name":"NIH","award":["R35 HL144481"],"award-info":[{"award-number":["R35 HL144481"]}]},{"name":"NIH","award":["R35HL176572"],"award-info":[{"award-number":["R35HL176572"]}]},{"name":"NIH","award":["T32GM007863"],"award-info":[{"award-number":["T32GM007863"]}]},{"award":["PFF Scholarship"],"award-info":[{"award-number":["PFF Scholarship"]}],"id":[{"id":"https:\/\/ror.org\/01cc8fr56","id-type":"ROR","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,7,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>Idiopathic pulmonary fibrosis (IPF) is a progressive, chronic lung disease with limited therapeutic options. Tryptophan metabolism is significantly dysregulated during lung fibrogenesis, with the metabolite kynurenine (kyn) accumulating in lung tissue and driving pathology via the aryl hydrocarbon receptor (AHR). This study evaluates the cell-specific contributions of kyn-mediated AHR signaling across different pulmonary cell types to clarify its role in disease progression.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Using a murine model of bleomycin-induced pulmonary fibrosis, lung tryptophan metabolites were profiled via liquid chromatography-mass spectrometry. The functional and transcriptomic impacts of kyn administration and AHR modulation were subsequently characterized across three distinct cellular compartments: CD103+ dendritic cells (DCs), fibroblasts, and alveolar epithelial cells (AECs).<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    Kyn levels were elevated in fibrotic lungs, and exogenous kyn selectively exacerbated collagen deposition during the fibrogenic phase rather than altering acute injury.\n                    <jats:italic>In vitro<\/jats:italic>\n                    monocultures of primary lung fibroblasts and AECs revealed negligible functional responses to kyn or AHR inhibition regarding myofibroblast differentiation, migration, or epithelial barrier disruption. Intriguingly, primary tissue-resident CD103+ DCs exhibited a hyperinflammatory, non-canonical AHR signaling profile\n                    <jats:italic>in vivo<\/jats:italic>\n                    . While\n                    <jats:italic>ex vivo<\/jats:italic>\n                    monoculture rapidly reverted these DCs to an anti-inflammatory, canonical AHR state, directly co-culturing DCs with fibrotic primary lung fibroblasts successfully restored the pathogenic, non-canonical signaling phenotype characterized by augmented IL-6 production and suppressed canonical targets.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>Pathogenic AHR signaling in pulmonary fibrosis is highly cell-context dependent and driven by complex cell-cell interactions. Reductionist monocultures fail to replicate tissue- level dendritic cell phenotypes, highlighting the necessity of co-culture models and providing a cautionary note for the systemic clinical use of AHR-targeted therapeutics.<\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.07.21.738475","type":"posted-content","created":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T04:10:12Z","timestamp":1784779812000},"source":"Crossref","is-referenced-by-count":0,"title":["Cell-Specific Modulation of the Aryl Hydrocarbon Receptor by Kynurenine in Pulmonary Fibrosis Requires Microenvironmental Crosstalk"],"prefix":"10.64898","author":[{"given":"Hannah","family":"Carter","sequence":"first","affiliation":[{"name":"Graduate Program of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, USA"},{"name":"Medical Scientist Training Program, University of Michigan, Ann Arbor, MI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin C.","family":"Anderson","sequence":"additional","affiliation":[{"name":"Graduate Program in Immunology, University of Michigan, Ann Arbor, MI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rita","family":"de Medina Costa","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua","family":"Franzen","sequence":"additional","affiliation":[{"name":"Graduate Program for Biological Chemistry, University of Michigan, Ann Arbor, MI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua","family":"Krukonis","sequence":"additional","affiliation":[{"name":"College of Language, Science, and Arts, University of Michigan, Ann Arbor, MI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kayla C.","family":"Jenkins","sequence":"additional","affiliation":[{"name":"Graduate Program in Immunology, University of Michigan, Ann Arbor, MI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rachel L.","family":"Zemens","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bethany B.","family":"Moore","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, USA"},{"name":"Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen J.","family":"Gurczysnki","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2026072705161442000_2026.07.21.738475v1.1","doi-asserted-by":"crossref","unstructured":"Martinez FJ , Collard HR , Pardo A , Raghu G , Richeldi L , Selman M , Swigris JJ , Taniguchi H , Wells AU . 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