Opposing T cell responses in experimental autoimmune encephalomyelitis

Naresha Saligrama, Fan Zhao, Michael J. Sikora, William S. Serratelli, Ricardo A. Fernandes, David M. Louis, Winnie Yao, Xuhuai Ji, Juliana Idoyaga, Vinit B. Mahajan, Lars M. Steinmetz, Yueh-Hsiu Chien, Stephen L. Hauser, Jorge R. Oksenberg, K. Christopher Garcia and Mark M. Davis ()
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Naresha Saligrama: Stanford University School of Medicine
Fan Zhao: Stanford University School of Medicine
Michael J. Sikora: Stanford University School of Medicine
William S. Serratelli: Stanford University School of Medicine
Ricardo A. Fernandes: Stanford University School of Medicine
David M. Louis: Stanford University School of Medicine
Winnie Yao: Stanford University School of Medicine
Xuhuai Ji: Stanford University School of Medicine
Juliana Idoyaga: Stanford University School of Medicine
Vinit B. Mahajan: Stanford University
Lars M. Steinmetz: Stanford University School of Medicine
Yueh-Hsiu Chien: Stanford University School of Medicine
Stephen L. Hauser: University of California
Jorge R. Oksenberg: University of California
K. Christopher Garcia: Stanford University School of Medicine
Mark M. Davis: Stanford University School of Medicine

Nature, 2019, vol. 572, issue 7770, 481-487

Abstract: Abstract Experimental autoimmune encephalomyelitis is a model for multiple sclerosis. Here we show that induction generates successive waves of clonally expanded CD4+, CD8+ and γδ+ 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 MOG35–55. 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.

Date: 2019
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DOI: 10.1038/s41586-019-1467-x

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