Abstract

NKT cells comprise three subsets—type I (invariant, iNKT), type II, and NKT-like cells, of which iNKT cells are the most studied subset. They are capable of rapid cytokine production after the initial stimulus, thus they may be important for polarisation of Th cells. Due to this, they may be an important cell subset in autoimmune diseases. In the current review, we are summarising results of NKT-oriented studies in major neurological autoimmune diseases—multiple sclerosis, myasthenia gravis, and Guillain-Barre syndrome and their corresponding animal models.

Highlights

  • CD1d-dependent while NKT-like are independent. iNKT cells express a restricted type of TCR (Vα24Jα18 Vβ11 in human, and Vα14Jα18 and Vβ8.2, Vβ7, or Vβ2 in mice), type II NKT cells express a wider array of TCR chains while the NKT-like has even more diverse TCR [1]. iNKT cells recognise α-galactosylceramide (α-GalCer) and some similar lipid-derivatives such as microbial α-glycuronylceramides or human self-antigen isoglobotrihexosylceramide [3]

  • CD1d or IFN-γplicate knockouts; in T cells and significantly exacerbates immunisation does not induce any significant changes in EAE course immunisation with either myelin basic protein (MBP) or Jahngoretseverity al., 2001[60]

  • Some pre-clinical studies on the murine models suggest that iNKT may be targeted to treat autoimmunity, including multiple sclerosis

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Summary

Introduction

They are capable of rapid cytokine production after the initial stimulus, they may be important for polarisation of Th cells. INKT cells recognise α-galactosylceramide (α-GalCer) and some similar lipid-derivatives such as microbial α-glycuronylceramides or human self-antigen isoglobotrihexosylceramide [3].

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