Whether antibody-mediated rejection after lung transplantation exists as an entity is debated by immunologists, histopathologists, and clinicians, without a strong consensus regarding diagnostic characteristics despite an increasing body of evidence that attests to a significant role in other solid organ transplant disciplines. Evidence for and against the protean manifestations of antibody-mediated rejection after lung transplantation is discussed, with special reference to hyperacute pulmonary allograft rejection as well as acute and chronic pulmonary allograft rejection, emphasizing the potential role of complement and antibodies to human leukocyte antigens and anti-endothelial antigens. A well-described clinical phenotype exists for hyperacute pulmonary allograft rejection with low-level evidence for efficacy of therapy with intravenous immunoglobulin, plasmapheresis, and anti-CD20 monoclonal antibodies plus supportive care, if instituted early in the evolution of the process. The clinical phenotype of acute antibody-mediated rejection is now better defined, if not widely diagnosed, and a similar treatment protocol appears effective. The role of antibody-mediated rejection in the development of chronic pulmonary allograft rejection remains an exciting area for further study based on some compelling preliminary work to date. Antibody-mediated rejection after lung transplantation remains a major area for research. In the clinical domain, experience suggests antibody-mediated rejection should be considered a potential cause of graft dysfunction, whether concomitant acute cellular rejection is diagnosed or not, and especially where resistance to corticosteroid therapy is encountered.