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.