The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Caspase-1–Processed Cytokines IL-1β and IL-18 Promote IL-17 Production by γδ and CD4 T Cells That Mediate Autoimmunity
Open accessAbstract
IL-1β plays a critical role in promoting IL-17 production by γδ and CD4 T cells. However, IL-1–targeted drugs, although effective against autoinflammatory diseases, are less effective against autoimmune diseases. Conversely, gain-of-function mutations in the NLRP3 inflammasome complex are associated with enhanced IL-1β and IL-18 production and Th17 responses. In this study, we examined the role of caspase-1–processed cytokines in IL-17 production and in induction of experimental autoimmune encephalomyelitis (EAE). Killed Mycobacterium tuberculosis, the immunostimulatory component in CFA used for inducing EAE, stimulated IL-1β and IL-18 production by dendritic cells through activation of the inflammasome complex and caspase-1. Dendritic cells stimulated with M. tuberculosis and myelin oligodendrocyte glycoprotein promoted IL-17 production by T cells and induced EAE following transfer to naive mice, and this was suppressed by a caspase-1 inhibitor and reversed by administration of IL-1β or IL-18. Direct injection of the caspase-1 inhibitor suppressed IL-17 production by CD4 T cells and γδ T cells in vivo and attenuated the clinical signs of EAE. γδ T cells expressed high levels of IL-18R and the combination of IL-18 and IL-23, as with IL-1β and IL-23, stimulated IL-17 production by γδ T cells, but also from CD4 T cells, in the absence of TCR engagement. Our findings demonstrate that caspase-1–processed cytokines IL-1β and IL-18 not only promote autoimmunity by stimulating innate IL-17 production by T cells but also reveal redundancy in the functions of IL-1β and IL-18, suggesting that caspase-1 or the inflammasome may be an important drug target for autoimmune diseases.
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Citations
Cites
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Self-citationInterleukin-18 Regulates Both Th1 and Th2 Responses
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Critical Regulation of Early Th17 Cell Differentiation by Interleukin-1 Signaling
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Cited by
A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases
Coll, R. C., Robertson, A. A. B., Chae, J. J., Higgins, S. C., Muñoz-Planillo, R., Inserra, M. C., Vetter, I., Dungan, L. S., Monks, B. G., Stutz, A., et al. (2015) · Nature Medicine · doi:10.1038/nm.3806 · Cited by 2,849
Self-citationOverview of the IL ‐1 family in innate inflammation and acquired immunity
Dinarello, C. A. (2018) · Immunological Reviews · doi:10.1111/imr.12621 · Cited by 1,866
Interleukin-1 and Related Cytokines in the Regulation of Inflammation and Immunity
Mantovani, A., Dinarello, C. A., Molgora, M., & Garlanda, C. (2019) · Immunity · doi:10.1016/j.immuni.2019.03.012 · Cited by 1,046
Interleukin-18 and IL-18 Binding Protein
Dinarello, C. A., Novick, D., Kim, S., & Kaplanski, G. (2013) · Frontiers in Immunology · doi:10.3389/fimmu.2013.00289 · Cited by 938
NLRP3 inflammasome and its inhibitors: a review
Shao, B.-Z., Xu, Z.-Q., Han, B.-Z., Su, D.-F., & Liu, C. (2015) · Frontiers in Pharmacology · doi:10.3389/fphar.2015.00262 · Cited by 836
“…and others has demonstrated that NLRP3 inflammasome activation contributes to progression of multiple sclerosis in humans and experimental autoimmune encephalomyelitis (EAE) in animal models (Ming et al., 2002; Jha et al., 2010; Lalor et al., 2011; Inoue et al., 2012a,b; Shao et al., 2014).”
Background
Metadata
- Authors
- Lalor, S. J., Dungan, L. S., Sutton, C. E., Basdeo, S. A., Fletcher, J. M., & Mills, K. H. G.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-05
- Volume
- 186
- Issue
- 10
- Pages
- 5738-5748
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1664996601
- Cited by
- 347
- References
- 34
- FWCI
- 12.11
- Type
- journal article
- Language
- en
- Open access
- bronze
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- The paper
- Lalor, S. J., Dungan, L. S., Sutton, C. E., Basdeo, S. A., Fletcher, J. M., & Mills, K. H. G. (2011). Caspase-1–Processed Cytokines IL-1β and IL-18 Promote IL-17 Production by γδ and CD4 T Cells That Mediate Autoimmunity. The Journal of Immunology. https://doi.org/10.4049/jimmunol.1003597
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