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Bronchiolitis obliterans syndrome (BOS), or its pathologic equivalent, obliterative bronchiolitis (OB), remains a major obstacle to long-term graft and patient survival after lung transplantation. Rapid-onset airway obstruction with subsequent stabilization, slow and inexorable decrease in airflow, or acute-onset respiratory insufficiency after years of normal lung function suggest a spectrum of graft–host responses to injury. 1 Although previous reviews have covered nomenclature, disease description, and risk factors of BOS, 2, 3 in this article, we will focus on the cellular mechanisms that cause rejection, although these remain somewhat elusive. Much of the basic knowledge of antigen recognition and of T-cell host response to injury has come from studies outside the field of lung allograft rejection. The current paradigm for the pathogenesis of OB has evolved from basic animal models and from clinical investigations …