title: Interplay of macrophages and T cells in the lung vasculature.
abstract: In severe pulmonary arterial hypertension (PAH), vascular lesions are composed of phenotypically altered vascular and inflammatory cells that form clusters or tumorlets. Because macrophages are found in increased numbers in intravascular and perivascular space in human PAH, here we address the question whether macrophages play a role in pulmonary vascular remodeling and whether accumulation of macrophages in the lung vasculature could be compromised by the immune system. We used the mouse macrophage cell line RAW 264.7 because these cells are resistant to apoptosis, have high proliferative capacity, and resemble cells in the plexiform lesions that tend to pile up instead of maintaining a monolayer. Cells were characterized by immunocytochemistry with cell surface markers (Lycopersicon Esculentum Lectin, CD117, CD133, FVIII, CD31, VEGFR-2, and S100). Activated, but not quiescent, T cells were able to suppress RAW 264.7 cell proliferative and migration activity in vitro. The carboxyfluorescein diacetate-labeled RAW 264.7 cells were injected into the naïve Sprague Dawley (SD) rat and athymic nude rat. Twelve days later, cells were found in the lung vasculature of athymic nude rats that lack functional T cells, contributing to vascular remodeling. No labeled RAW 264.7 cells were detected in the lungs of immune-competent SD rats. Our data demonstrate that T cells can inhibit in vitro migration and in vivo accumulation of macrophage-like cells.
authors.affiliation: Department of Pediatrics, University of Colorado Denver, 12700 E. 19th Ave, Aurora, CO 80045, USA.
authors.forename: Evgenia
authors.initials: E
authors.lastname: Gerasimovskaya
authors.forename: Adelheid
authors.initials: A
authors.lastname: Kratzer
authors.forename: Asya
authors.initials: A
authors.lastname: Sidiakova
authors.forename: Jonas
authors.initials: J
authors.lastname: Salys
authors.forename: Martin
authors.initials: M
authors.lastname: Zamora
authors.forename: Laimute
authors.initials: L
authors.lastname: Taraseviciene-Stewart
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000032:analysis; D002450:Cell Communication / Q000276:immunology*; D002460:Cell Line; D002465:Cell Movement / Q000276:immunology; D049109:Cell Proliferation; D065627:Familial Primary Pulmonary Hypertension; D005452:Fluoresceins; D005456:Fluorescent Dyes; D006976:Hypertension, Pulmonary / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D008168:Lung / Q000098:blood supply* / Q000166:cytology / Q000276:immunology; D008264:Macrophages / Q000166:cytology* / Q000276:immunology / Q000637:transplantation; D008297:Male; D051379:Mice; D008954:Models, Biological; D011651:Pulmonary Artery / Q000166:cytology* / Q000276:immunology; D051381:Rats; D011923:Rats, Nude; D017207:Rats, Sprague-Dawley; D013601:T-Lymphocytes / Q000166:cytology* / Q000276:immunology
chemical_list: D015415:Biomarkers; D005452:Fluoresceins; D005456:Fluorescent Dyes; C027780:carboxyfluoresceindiacetate