In this article we have reviewed the main cellular aspects of PDI-mediated host pathogen interactions and the pathways that are involved in viral, bacterial (including bacterial toxins), and parasitic infections. A number of cellular mechanisms through which PDI modulates some specific cellular pathways in immune cells have been described, such as redox-sensitive attachment, antigen presentation in the ER and exit from it, and association to phagosome and ROS production by NADPH oxidase (Figure 2 ). Many of these responses are antigen-specific and the precise mechanisms of action remain to be fully elucidated, especially in the context of redox changes in cross-presentation phenomena. Moreover, little is known about the role of PDI in infection per se, as well as how PDI signals to a more integrated cellular response to stress [63] . PDI global knockout mice are only viable until birth, but partial gene-modified mice and also modified pathogens will help to reveal the significant redox role of PDI and its redox partners. Overall, PDI is a key regulator that may propagate or limit the severity of the infection processes, depending on the infectious organism involved. A better understanding of these complex regulatory steps will provide insightful information on the redox role and coevolutional biological process, and assist the development of more specific therapeutic strategies in pathogen-mediated infections.