Journal
NATURE
Volume 572, Issue 7770, Pages 481-+Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41586-019-1467-x
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Funding
- NIH [S10OD018220]
- National Multiple Sclerosis Society (NMSS)
- NMSS [RG-1611-26299]
- Ovarian Cancer Research Fund Alliances
- US National Institutes of Health (NIH) [1DP2AR069953]
- Wellcome Trust [WT101609MA]
- US NIH [U19 AI057229, R01AI103867]
- Howard Hughes Medical Institute
- Mathers Foundation
- Simons Foundation
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Experimental autoimmune encephalomyelitis is a model for multiple sclerosis. Here we show that induction generates successive waves of clonally expanded CD4(+), CD8(+) and gamma delta(+) T cells in the blood and central nervous system, similar to gluten-challenge studies of patients with coeliac disease. We also find major expansions of CD8(+) T cells in patients with multiple sclerosis. In autoimmune encephalomyelitis, we find that most expanded CD4(+) T cells are specific for the inducing myelin peptide MOG(35-55). By contrast, surrogate peptides derived from a yeast peptide major histocompatibility complex library of some of the clonally expanded CD8(+) T cells inhibit disease by suppressing the proliferation of MOG-specific CD4(+) T cells. These results suggest that the induction of autoreactive CD4(+) T cells triggers an opposing mobilization of regulatory CD8(+) T cells.
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