4.8 Article

High Interferon-γ Uniquely in Vδ1 T Cells Correlates with Markers of Inflammation and Axonal Damage in Early Multiple Sclerosis

Journal

FRONTIERS IN IMMUNOLOGY
Volume 8, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2017.00260

Keywords

cerebrospinal fluid; gamma-delta T cells; interferon-gamma; multiple sclerosis; natalizumab; Vdelta1 T cells

Categories

Funding

  1. Swedish Research Council
  2. Sahlgrenska Academy
  3. LUA-ALF
  4. NEURO Sweden
  5. Swedish Foundation for MS Research
  6. Adlerbert Research Foundation
  7. Wilhelm and Martina Lundgrens Science Foundation
  8. European Research Council
  9. Knut and Alice Wallenberg Foundation
  10. Swedish Society of the Neurologically Disabled
  11. Research Foundation of the Multiple Sclerosis Society of Gothenburg
  12. Edit Jacobsons Foundation
  13. Helena Ahlin's Foundation
  14. Novartis
  15. Swedish Brain Foundation
  16. Biogen

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We have identified a population of T lymphocytes in peripheral blood, V delta 1 TCR gamma delta T lymphocytes, which unexpectedly was uniquely expressing high production of interferon-gamma in newly diagnosed, untreated multiple sclerosis (MS) patients. IFN-gamma production in this population distinctly correlated to parameters of clinical disease activity, inflammation, and neuronal damage. These V delta 1 T lymphocytes belong to a population of innate T lymphocytes that recognize antigen in the context of CD1d/CD1c and which include reactivity to the myelin glycosphingolipid sulfatide. Importantly, patients treated with natalizumab, blocking leukocyte transmigration to central nervous system, had completely normalized levels of interferon-gamma-producing V delta 1 T lymphocytes. A biomarker and early sign of demyelinating disease in MS is much warranted and would help identify immunopathogenesis and prognosis of disease as well as monitor success with adequate treatment. The present study identifies the V delta 1 T lymphocytes as an early marker of MS and a possible link to understanding the disease etiology.

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