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  3. Opposing T cell responses in experimental autoimmune encephalomyelitis

Opposing T cell responses in experimental autoimmune encephalomyelitis

  • Nature. 2019 Aug;572(7770):481-487. doi: 10.1038/s41586-019-1467-x.
Naresha Saligrama 1 2,  Fan Zhao # 1,  Michael J Sikora # 3,  William S Serratelli 2,  Ricardo A Fernandes 4,  David M Louis 2,  Winnie Yao 2,  Xuhuai Ji 5,  Juliana Idoyaga 1,  Vinit B Mahajan 6 7,  Lars M Steinmetz 3 8 9,  Yueh-Hsiu Chien 1 2 10,  Stephen L Hauser 11,  Jorge R Oksenberg 11,  K Christopher Garcia 4 12 13,  Mark M Davis 14 15 16
Affiliations

Affiliations

  • 1 Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, USA.
  • 2 Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA.
  • 3 Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
  • 4 Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA, USA.
  • 5 Human Immune Monitoring Center, Stanford University School of Medicine, Stanford, CA, USA.
  • 6 Byers Eye Institute, Department of Ophthalmology, Stanford University, Palo Alto, CA, USA.
  • 7 Veterans Affairs Palo Alto Health Care, Palo Alto, CA, USA.
  • 8 Stanford Genome Technology Center, Stanford University, Palo Alto, CA, USA.
  • 9 European Molecular Biology Laboratory (EMBL), Genome Biology Unit, Heidelberg, Germany.
  • 10 Program in Immunology, Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA.
  • 11 Department of Neurology and UCSF Weill Institute for Neurosciences, University of California, San Francisco, CA, USA.
  • 12 Department of Structural Biology, Stanford University School of Medicine, Stanford, CA, USA.
  • 13 The Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA, USA.
  • 14 Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA, USA. mmdavis@stanford.edu.
  • 15 Institute of Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA, USA. mmdavis@stanford.edu.
  • 16 The Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA, USA. mmdavis@stanford.edu.
  • # Contributed equally.
PMID: 31391585 DOI: 10.1038/s41586-019-1467-x
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.

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