Projects per year
Abstract
Mice lacking IL-6 are resistant to autoimmune diseases, such as experimental autoimmune encephalomyelitis (EAE), which is driven by CNS-reactive CD4(+) T cells. There are multiple cellular sources of IL-6, but the critical source in EAE has been uncertain. Using cell-specific IL-6 deficiency in models of EAE induced by active immunization, passive transfer, T cell transfer, and dendritic cell transfer, we show that neither the pathogenic T cells nor CNS-resident cells are required to produce IL-6. Instead, the requirement for IL-6 was restricted to the early stages of T cell activation and was entirely controlled by dendritic cell-derived IL-6. This reflected the loss of IL-6R expression by T cells over time. These data explain why blockade of IL-6R only achieves protection against EAE if used at the time of T cell priming. The implications for therapeutic manipulation of IL-6 signaling in human T cell-driven autoimmune conditions are considered.
Original language | English |
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Pages (from-to) | 881-885 |
Number of pages | 5 |
Journal | The Journal of Immunology |
Volume | 190 |
Issue number | 3 |
DOIs | |
Publication status | Published - 1 Feb 2013 |
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Dive into the research topics of 'Cutting Edge: IL-6-Dependent Autoimmune Disease: Dendritic Cells as a Sufficient, but Transient, Source'. Together they form a unique fingerprint.Projects
- 2 Finished
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PhD STUDENT - JOANNE SIMPSON - Supervisor MOHINI GRAY
Iredale, J. (Principal Investigator)
1/09/12 → 31/08/16
Project: Research
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Immune cell interactions in the inflammed CNS
Anderton, S. (Principal Investigator) & O'Connor, R. (Co-investigator)
1/04/09 → 30/09/14
Project: Research