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Lung transplantation is the optimal treatment for selected patients with end-stage chronic lung diseases. However, chronic lung allograft dysfunction remains the leading obstacle to improved long-term outcomes. Traditionally, lung allograft rejection has been considered primarily as a manifestation of cellular immune responses. However, in reality, an array of complex, interacting and multifactorial mechanisms contribute to its emergence. Alloimmune-dependent mechanisms, including T-cell-mediated rejection and antibody-mediated rejection, as well as non-alloimmune injuries, have been implicated. Moreover, a role has emerged for autoimmune responses to lung self-antigens in the development of chronic graft injury. The aim of this review is to summarise the immune processes involved in the pathogenesis of chronic lung allograft dysfunction, with advanced insights into the role of innate immune pathways and crosstalk between innate and adaptive immunity, and to identify gaps in current knowledge., Competing Interests: Conflict of interest: S. Bos has nothing to disclose. Conflict of interest: L. Milross has nothing to disclose. Conflict of interest: A.J. Filby has nothing to disclose. Conflict of interest: R. Vos reports grants from Research Foundation-Flanders (FWO), outside the submitted work. Conflict of interest: A.J. Fisher reports grants from GlaxoSmithKline, grants, personal fees and non-financial support from Mallinckrodt Pharmaceuticals, personal fees from Altavant, and grants from Pfizer, outside the submitted work., (Copyright ©The authors 2022.)