Abstract
metalloproteases (MMPs) MMP-9 and MMP-2 in the lungs of immunized animals when compared with control rat lungs. Anti– endothelial cell antibodies recognize several endothelial cell epitopes, including vascular endothelial growth factor receptor (VEGFR)-2 and angiotensin-converting enzyme (ACE). Mice injected with anti–endothelial cell serum also develop emphysema. Lung morphometry of mice injected with anti–endothelial cell antibody showed 20% enlargement of alveolar airspaces over a 5-wk period as compared with normal rat serum–injected controls. Immunization also causes accumulation of CD4 T cells in the lung. Adoptive transfer of a pathogenic, spleenderived CD4 cell population into naive immune-competent animals also results in emphysema. Moreover, adoptive transfer of CD4 spleen cells into secondary syngeneic rats resulted in emphysema, even though these secondary rats had not been immunized with human umbilical vein endothelial cells (HUVEC). In this study, we show for the first time that humoral and CD4 cell–dependent mechanisms are sufficient to trigger the development of emphysema. Our data demonstrate that pathogenic CD4 T lymphocytes are necessary and sufficient in breaking a regulatory tolerance and causing emphysema in naive immunecompetent rats, suggesting the involvement of autoimmune mechanisms in alveolar septal cell destruction.
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