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Original Articles: General Thoracic

Invited Commentary

Division of Thoracic Surgery, Massachusetts General Hospital, 55 Fruit St, Blake 1570, Boston, MA 02114

(Email: jallan{at}partners.org).

McCourtie and colleagues [1] have shown that alveolar macrophages and pulmonary artery endothelial cells produce mutually reinforcing proinflammatory cytokine responses to lung ischemia and reperfusion. These data expand our understanding of the mechanisms that determine the magnitude of the inflammatory response that occurs subsequent to lung transplantation.

The early immune response to an allograft consists of two basic components: (1) generalized inflammation associated with the activation of the innate immune system and (2) alloantigen-specific responses of the acquired immune system. During the past decade, there has been a growing recognition that the antigenicity and immunogenicity of a graft are greatly influenced by the inflammatory milieu, above and beyond the genetically determined antigen disparities inherent in an allotransplant. Proinflammatory states are known to upregulate the expression of adhesion molecules, costimulatory molecules, and major histocompatibility antigens, with the net effect of supporting the cognate interactions of T cells with directly or indirectly presented alloantigens. Moreover, recent data from our group and others suggest that a proinflammatory state is detrimental to the induction of transplantation tolerance in both small and large animal models that rely on primarily on peripheral (regulatory) mechanisms of tolerance.

The data presented here emphasize the need to address the alveolar macrophage in strategies intending to abrogate inflammation in the pulmonary allograft. These data also remind us that although there are many similarities among the various solid-organ transplants, important organ-specific differences need to be considered in the pursuit of improved outcomes.

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1. McCourtie AS, Merry HE, Farivar AS, Goss CH, Mulligan MS. Alveolar macrophage secretory products augment the response of rat pulmonary artery endothelial cells to hypoxia and reoxygenation Ann Thorac Surg 2008;85:1056-1060.[Abstract/Free Full Text]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): James S. Allan Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Allan, J. S. Search for Related Content PubMed PubMed Citation Articles by Allan, J. S. Related Collections Lung - other Related Article