CONCLUSIONS AND PERSPECTIVES
Programmed cell death (PCD) in its different modes of presentation and acting through different pathways has proved to be more that the final fate of a damaged or a senescent cell. This is a complex process which can be induced, sustained, adjusted and even reversed according to the cell type, the intra and extracellular conditions, the stimulus that triggers it and the interactions with other surrounding cells. Several experimental data have demonstrated that PCD is actively involved in a variety of biological functions but especially in innate immunity and host defense. As it has been discussed throughout this review, PCD is induced by pathogen presence and is part of the immune mechanisms involved in their detection and elimination. Different types of pathogens are able to induce different cell death modalities, indicating that is a specialized process rather than just a physiological consequence of microbe invasion to host cells. PCD is no longer seen as the result of an inflammatory process but also as fine-tuned mechanism that can induce, amplify or modulate this inflammation, either during physiological or pathological conditions, including infection and malignant transformation. The expanding network of cell death programs is revealing novel and complex variants or PCD and their key role in innate immunity and immune cell homeostasis. The existence of multiple forms for a cell to die and their involvement in different immune mechanisms offers interesting ways to selectively modulate and enhance immune response to infections, chronic inflammation and cancer, through pharmacological interventions and immunotherapy.