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Purpose of review This review presents a concise update on clinical donation after cardiac death (DCD or DDCD) lung transplantation. Lung allografts have predominantly been procured from donors after determination of neurologic death but will not meet the existing demand. A steadily increasing need for lungs is evident worldwide, especially in an era of improved outcomes for recipients. Other solid organ utilization from donors after determination of cardiac death has markedly increased internationally, but the utilization rate of lungs from such donors is still considerably less. The multifaceted reasons for this discrepancy are considered, and the recent evidence available supporting DCD for lung transplantation in clinical practice is presented in context. The recent experimental research studies are not within the remit of this appraisal. Recent findings The more recent and markedly increased lung recipient cohorts showed very satisfactory survival outcomes for DCD transplantation in several programs. The overall utilization rate, however, remains low. The background and the rationale of lung donor allograft expansion to proactively include DCD allografts from controlled (Maastricht category III donors) is re-emphasized in this review. The feasibility of other DCD categories for lung transplantation is considered. This is particularly prudent with the advent of the ex-vivo lung perfusion modality in pulmonary procurement. Summary Despite evidence for adequate survival outcomes and reported favorable primary graft dysfunction rates, DCD lung transplantation remains underutilized in most countries. Waiting times could be notably reduced and mortality of lung candidates arguably decreased by a more decided and appropriate implementation of proven DCD lung transplant strategies.

Lung transplantation is now a well established treatment option for several end-stage respiratory diseases. Survival after lung transplantation has significantly improved over the last decade. The primary limitation to increased utilization of lung transplantation remains donor scarcity. Suitable allografts have been procured from donors after determination of neurologic death and from donors after determination of cardiac death (DDCD or DCD). Historically, the first human lung transplantation performed, utilized an allograft procured after cardiovascular death, also referred to as nonheart-beating donor.The experience at University of Wisconsin in 1993 reintroduced DCD lung transplantation with the first successful clinical case.A potential additional lung allograft source, DCD lung transplantation has been established with very acceptable outcomes observed by several centers. We provide the relevant background for the rationale of donor allograft expansion to include DCD lungs from controlled (Maastricht category III donors).This review considers the available evidence for DCD lung transplantation and compares reported primary graft dysfunction rates and current survival data available.

Rat lung allograft rejection is mediated by collagen type V (col(V)) specific T-helper-cell 17 (Th17) cells. Adoptive transfer of these cells is sufficient to induce rejection pathology in isografts, whereas tolerance to col(V) suppresses allograft rejection. Therefore, we tested whether regulatory T cells from tolerant rats could suppress the Th17-mediated rejection in the syngeneic model of lung transplantation.Rats were subjected to syngeneic left lung transplantation, and acute rejection was induced by adoptive transfer of lymph node cells from col(V)-immunized rats. Tolerance was induced by intravenous injection of col(V), and spleen lymphocytes were used for adoptive transfer. CD4+ T cells were depleted using magnetic beads. Lung isografts were analyzed using micro-positron emission tomography imaging and histochemistry. The transvivo delayed type hypersensitivity assay was used to analyze the Th17 response.Adoptive cotransfer of col(V)-specific effector cells with cells from col(V)-tolerized rats suppressed severe vasculitis and bronchiolitis with parenchymal inflammation, and the expression of interleukin (IL)-17 transcripts in mediastinal lymph nodes induced by effector cells alone. Analysis by transvivo delayed type hypersensitivity showed that the reactivity to col(V) was dependent on the presence of tumor necrosis factor-alpha and IL-17 but not interferon-gamma. Depletion of CD4+ T cells from the suppressor cell population abrogated the col(V)-specific protection.Th17-mediated acute rejection after lung transplantation is ameliorated by CD4+ col(V)-specific regulatory T cells. The mechanism for this Th17 suppression is consistent with tolerance induction to col(V). The goal of transplantation treatment, therefore, should target Th17 development and not suppression of T-cell activation by suppressing IL-2.