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Cardiac allograft rejection is an active process that is preceded by an inflammatory phase, which is triggered by the innate immune system. We studied the expression of the microtubule-associated protein 1A/1B-light chain 3 (LC3), a mammalian homologue of yeast Atg8, a protein important in the autophagy process. Long-term survival of cardiac allografts in mice is associated with an immune privilege which can be reversed, resulting in graft rejection. The immune privilege is characterized by decreased expression of cytokines and chemokines that promote delayed-type hypersensitivity (DTH), decreased lymphocyte infiltration, decreased macrophage and dendritic cell infiltration, and decreased endothelial cell activation. Thus, it is of interest to determine the expression pattern of proteins involved in a number of these functions and to determine whether their expression is altered in rejecting cardiac allografts. Transgenic mice that express the LC3 transgene under the control of the mouse metallothionein promoter were used to detect differential expression of LC3 during cardiac allograft rejection and inflammation. Confirmation was obtained by immunohistochemical studies of rejecting and inflamed allografts. Increased expression of LC3 in infiltrating cells at the site of allograft rejection suggests autophagy involvement, as activation of autophagy promotes the degradation of cytoplasmic proteins and organelles. This is a novel finding that suggests that autophagy is not only a protective mechanism against apoptosis, but also that it participates in the inflammatory process. Our findings