Original articleGeneral thoracicAntibodies to Self-Antigens Predispose to Primary Lung Allograft Dysfunction and Chronic Rejection
Section snippets
Study Subjects
Adult patients undergoing lung transplantation at Washington University Medical Center, Barnes-Jewish Hospital were prospectively enrolled in the study between 1995 and 2005 after obtaining informed consent, in accordance with a protocol approved by the Institutional Review Board. The peripheral blood mononuclear cells were isolated from heparinized blood by Ficoll-Hypaque density gradient centrifugation (Pharmacia, Stockholm, Sweden), and stored at −135°C. The plasma separated from peripheral
Pretransplant Antibodies and Risk of PGD
The study included 142 lung transplant patients. The clinical and demographic profile of the recipients and donors is shown in Table 1. Of the patients included in the study, 101 were negative for all antibodies, and 41 had one or more of the three antibodies (Fig 1). There were no significant differences in the clinicodemographic variables between the study groups. We first screened BAL from HLA-antibody negative patients with (n = 28) and without PGD (n = 17) for soluble C4d. Patients with
Comment
Land and colleagues [12] initially introduced the concept of “response to injury” hypothesis [13]. They proposed the role for early posttransplant inflammation in increasing allograft immunogenicity and risk for chronic rejection. In human lung transplantation, PGD is known to be a major risk factor for BOS [3]. All grades of PGD (1 to 3) independently increase the risk. The reported incidence of PGD after lung transplantation approaches more than 80% [3]. As PGD is a major risk for BOS, it is
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