Journal
NATURE BIOTECHNOLOGY
Volume 37, Issue 3, Pages 238-251Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41587-019-0015-4
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Funding
- Canadian Institutes of Health Research (CIHR)
- Diabetes Canada
- Crohn's and Colitis Foundation of Canada
- Multiple Sclerosis Society of Canada (MSSC)
- ISCIII
- FEDER [PIE14/00027, PI15/0797]
- NEURON-ERANET (European Research Projects on Neuroinflammation) [NEURON7-FP-715-018]
- Ministerio de Economia y Competitividad of Spain (MINECO)
- Generalitat de Catalunya (SGR Programme)
- Generalitat de Catalunya (CERCA Programme)
- JDRF Career Development Award
- Diabetes Association (Foothills)
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The main function of the immune system in health is to protect the host from infection by microbes and parasites. Because immune responses to nonself bear the risk of unleashing accidental immunity against self, evolution has endowed the immune system with central and peripheral mechanisms of tolerance, including regulatory T and B cells. Although the past two decades have witnessed the successful clinical translation of a whole host of novel therapies for the treatment of chronic inflammation, the development of antigen-based approaches capable of selectively blunting autoimmune inflammation without impairing normal immunity has remained elusive. Earlier autoantigen-specific approaches employing peptides or whole antigens have evolved into strategies that seek to preferentially deliver these molecules to autoreactive T cells either indirectly, via antigen-presenting cells, or directly, via major histocompatibility complex molecules, in ways intended to promote clonal deletion and/or immunoregulation. The disease specificity, mechanistic underpinnings, developability and translational potential of many of these strategies remain unclear.
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