{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T14:38:12Z","timestamp":1784299092275,"version":"3.55.0"},"reference-count":174,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2022,7,12]],"date-time":"2022-07-12T00:00:00Z","timestamp":1657584000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Lung transplant\u00a0remains\u00a0a key therapeutic\u00a0option\u00a0for patients with end stage lung disease but short- and long-term survival lag other solid organ transplants. Early ischemia-reperfusion injury in the form of primary graft dysfunction (PGD) and\u00a0acute\u00a0cellular rejection are risk factors for chronic lung allograft dysfunction (CLAD), a syndrome of airway and parenchymal fibrosis that is the major barrier to long term survival.\u00a0An increasing\u00a0body\u00a0of research suggests lymphocytic airway\u00a0inflammation plays a significant role in these important clinical syndromes.\u00a0Cytotoxic\u00a0T cells are observed in airway rejection,\u00a0and transcriptional analysis of airways reveal common cytotoxic gene patterns across solid organ transplant rejection.\u00a0Natural killer (NK) cells have also\u00a0been implicated in the early allograft damage response to PGD, acute rejection,\u00a0cytomegalovirus,\u00a0and\u00a0CLAD. This review\u00a0will\u00a0examine\u00a0the roles of lymphocytic airway inflammation across the lifespan of the allograft, including:\u00a01)\u00a0The\u00a0contribution\u00a0of innate lymphocytes\u00a0to\u00a0PGD\u00a0and the impact of PGD on the adaptive immune response.\u00a02)\u00a0Acute cellular rejection pathologies and the limitations in identifying airway inflammation by transbronchial biopsy.\u00a03) Potentiators of airway inflammation\u00a0and heterologous immunity,\u00a0such as\u00a0respiratory\u00a0infections, aspiration,\u00a0and the airway microbiome.\u00a04)\u00a0Airway contributions to CLAD pathogenesis, including epithelial to\u00a0mesenchymal\u00a0transition (EMT),\u00a0club cell loss,\u00a0and\u00a0the\u00a0evolution from constrictive bronchiolitis to parenchymal fibrosis.\u00a05)\u00a0Protective mechanisms of fibrosis involving\u00a0regulatory T cells.\u00a0In summary,\u00a0this review\u00a0will examine our current understanding of the complex interplay between the transplanted airway epithelium, lymphocytic\u00a0airway\u00a0infiltration, and\u00a0rejection\u00a0pathologies.<\/jats:p>","DOI":"10.3389\/fimmu.2022.908693","type":"journal-article","created":{"date-parts":[[2022,7,12]],"date-time":"2022-07-12T10:01:14Z","timestamp":1657620074000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":12,"title":["Lymphocytic Airway Inflammation in Lung Allografts"],"prefix":"10.3389","volume":"13","author":[{"given":"Jesse","family":"Santos","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel R.","family":"Calabrese","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John 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