About this Research Topic
Gamma delta T-cells (γδT cells) have been characterised by the expression of a γδ T-cell receptor (TCR). When the γδ TCR and the corresponding αβ TCR were first discovered it was assumed that the corresponding cell types were likely to be functionally very similar. However, some 30 years later, we have realised that they are not. Unlike αβT-cells, γδT-cells (i) sense target antigens independent of MHC molecules; (ii) display NK-cell like innate reactivities, including killing of infected cells as well as microbes; (iii) are able to take up large particulates, including bacteria, and (iv) can act as professional antigen presenting cells.
The ‘stress sensing’ abilities of γδ T cells have led to a great interest in exploring their potential use in novel immunotherapies, not least in cancer. In addition, their capacity to produce various cytokines and to interact with other cells, such as lymphocytes, myeloid cells and neutrophils, has raised an interest in their potential therapeutic use as immunomodulators. γδ T cells have therefore recently come to stand out as a distinctly unique cell type. At the same time, we have come to realise that γδ T cells are likely to be an ancient cell type with ancestors as far back as in our common ancestors to jawless fish and thereby, potentially predating the development of our adaptive immune system.
It is clear that to make full use of the great potential of γδ T cells in immunotherapeutic interventions, we must significantly improve our understanding of the extensive plasticity and multifunctionality of γδ T cells and of how these cells can be harnessed therapeutically, both safely and effectively.
In this Research Topic, we welcome the submission of Review, Original Research and Methods articles, in the area of γδ T cell plasticity and multifunctionality, primarily focusing on how an increased knowledge in this area can be used and developed further towards improved immunotherapeutic applications in cancer, infectious disease, autoimmunity and other immunity-related areas. We welcome contributions that cover, but are not limited to, the following topics:
1. γδT cell recognition of transformed or infected cells as well as of pathogens themselves.
2. γδT cell killing mechanisms of infected cells and transformed cells.
3. γδT cell communication with other cells following recognition and killing events.
4. Mechanisms by which γδT cells take up killed pathogens or cells and process and present peptide antigens from these to other T cells.
5. When and how did γδT cells and their ancestral and related cells evolve these recognition, killing, uptake and antigen presenting capabilities.
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