The role of invariant NKT cells in organ-specific autoimmunity

Caterina Di Pietro, Marika Falcone

Research output: Contribution to journalArticle

Abstract

Invariant NKT cells (iNKT) represent a unique subset of innate lymphocytes that play a dual role and exert a pro-inflammatory function and also a tolerogenic function that is crucial to maintain T cell tolerance and prevent autoimmune diseases like Multiple Sclerosis, Type 1 Diabetes, Rheumatoid Arhritis and Systemic Lupus Erithematosus (SLE). Although a large body of evidence indicated that iNKT cells are instrumental to counterregulate T cell-mediated autoimmune diseases, there is still some controversy on whether iNKT cells can actively induce immunosuppression and directly dampen T cell autoimmunity. Moreover, the recent discovery of a distinct iNKT cell subset, the iNKT17 cells, with strong adjuvant and pro-inflammatory function raised the question on what is the role of NKT17 cells in the pathogenesis of autoimmune diseases. Here, we review the current knowledge on iNKT cell biology and focus our attention on the possible mechanism of action and final effect of the different iNKT cell subsets in the pathogenesis of T cellmediated autoimmune diseases.

Original languageEnglish
Pages (from-to)1240-1250
Number of pages11
JournalFrontiers in Bioscience
Volume19
Issue number8
DOIs
Publication statusPublished - Jun 1 2014

Fingerprint

Natural Killer T-Cells
Autoimmunity
T-cells
Autoimmune Diseases
Cytology
T-Lymphocytes
Lymphocytes
Medical problems
Lymphocyte Subsets
Type 1 Diabetes Mellitus
Immunosuppression
Multiple Sclerosis
Cell Biology

Keywords

  • Autoimmune diseases
  • Cytokines
  • Dendritic cells
  • Immune tolerance
  • Natural killer T cells
  • Review

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)
  • Medicine(all)

Cite this

The role of invariant NKT cells in organ-specific autoimmunity. / Di Pietro, Caterina; Falcone, Marika.

In: Frontiers in Bioscience, Vol. 19, No. 8, 01.06.2014, p. 1240-1250.

Research output: Contribution to journalArticle

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