Abstract |
Growing awareness of the multiplicity of roles for the IL-1 family in immune regulation has prompted research exploring these cytokines in the context of vaccine-induced immunity. While tightly regulated, cytokines of the IL-1 family are normally released in response to cellular stress and in combination with other danger-/damage-associated molecular patterns (DAMPs), triggering potent local and systemic immune responses. In the context of infection or autoimmunity, engagement of IL-1 family receptors links robust innate responses to adaptive immunity. Clinical and experimental evidence has revealed that many vaccine adjuvants induce the release of one or multiple IL-1 family cytokines. The coordinated release of IL-1 family members in response to adjuvant-induced damage or cell death may be a determining factor in the transition from local inflammation to the induction of an adaptive response. Here, we analyse the effects of IL-1 family cytokines on innate and adaptive immunity with a particular emphasis on activation of antigen-presenting cells and induction of T cell-mediated immunity, and we address in detail the contribution of these cytokines to the modes of action of vaccine adjuvants including those currently approved for human use.
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Authors | Natalia Muñoz-Wolf, Ed C Lavelle |
Journal | The FEBS journal
(FEBS J)
Vol. 285
Issue 13
Pg. 2377-2401
(07 2018)
ISSN: 1742-4658 [Electronic] England |
PMID | 29656546
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Copyright | © 2018 Federation of European Biochemical Societies. |
Chemical References |
- Adjuvants, Immunologic
- Cytokines
- Interleukin-1
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Topics |
- Adaptive Immunity
(drug effects, immunology)
- Adjuvants, Immunologic
(pharmacology)
- Animals
- Antigen-Presenting Cells
(drug effects, immunology, metabolism)
- Cytokines
(immunology, metabolism)
- Humans
- Immunity, Innate
(drug effects, immunology)
- Interleukin-1
(immunology, metabolism)
- Stress, Physiological
(drug effects, immunology)
- T-Lymphocytes
(drug effects, immunology, metabolism)
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