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This phenomenon occurs in both connective tissue disease\u2013associated ILD and, surprisingly, idiopathic pulmonary fibrosis (IPF), where immune-driven pathogenesis is controversial.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To determine whether immune responses in the lung LNs of patients with ILD are antigen-specific and significant to pathology and etiology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>ILD lung LNs excised at transplant (30 IPF, 7 interstitial pneumonia with autoimmune features, 4 hypersensitivity pneumonitis, 5 connective tissue disease\u2013associated ILD, 5 other ILD) and 36 donor control lung LNs were analyzed by spectral flow cytometry. Formalin-fixed lung LNs and OCT-fixed lung samples of patients with IPF were used to determine germinal center (GC) and antigen-specific responses. Serum autoantibody responses were measured by radioligand binding assay.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>All patients with ILD revealed a common adaptive immune landscape of antigen responses in lung LNs characterized by the presence of GC B cells, T follicular helper cells, and activated T cells. Immunological synapses identified in the lung LNs demonstrated that antigen stimulation is ongoing in patients with ILD. Lung LN frequencies of T follicular helper and T regulatory cells correlated with circulating antibody concentrations to ABLIM1, a recently identified autoantigen expressed widely, including in aberrant basaloid cells that are uniquely found in fibrotic lungs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Antigen-induced activation and development of GC in enlarged lung LNs represents a shared immunopathologic mechanism associated with progressive pulmonary fibrosis among patients with ILD, regardless of etiology. Autoantigens overexpressed in progressive pulmonary fibrosis may be key drivers of these GC responses.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202502-0419oc","type":"journal-article","created":{"date-parts":[[2025,8,15]],"date-time":"2025-08-15T19:04:50Z","timestamp":1755284690000},"page":"1823-1834","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":9,"title":["Active Antigen-Specific Adaptive Immune Responses Are Shared among Patients with Progressive Fibrotic Interstitial Lung Disease"],"prefix":"10.1093","volume":"211","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9333-1356","authenticated-orcid":false,"given":"Tania E.","family":"Velez","sequence":"first","affiliation":[{"name":"Division of Pulmonary and Critical Care Medicine, Department of Medicine, 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