CD3-CD56+ NK cells display an inflammatory profile in RR-MS patients

Ilhan Tahrali1, Umut Can Kucuksezer1, Nilgun Akdeniz1

  • 1Istanbul University, Aziz Sancar Institute of Experimental Medicine, Department of Immunology, Istanbul, Turkey.

Immunology Letters
|October 8, 2019
PubMed

Insights

Interferon-beta (IFN-β) therapy for relapsing-remitting Multiple Sclerosis (RR-MS) may increase Natural Killer (NK) cell pro-inflammatory activity. This study found elevated activating receptors and Interleukin-22 (IL-22) in RR-MS patients on IFN-β.

Area of Science:

  • Immunology
  • Neuroimmunology
  • Cellular Biology

Background:

  • Multiple Sclerosis (MS) is a central nervous system disease involving immune-mediated and neurodegenerative processes.
  • Relapsing-remitting MS (RR-MS) is the most common form, characterized by acute attacks and remissions.
  • First-line treatments for RR-MS include interferon-beta (IFN-β) and glatiramer acetate.

Purpose of the Study:

  • To investigate the expression of activating and inhibitory receptors on Natural Killer (NK) cells.
  • To measure Interleukin-22 (IL-22) levels in RR-MS patients.
  • To compare NK cell profiles in RR-MS patients with and without IFN-β therapy.

Main Methods:

  • Flow cytometry was used to analyze NK cell receptor expression.
  • Interleukin-22 (IL-22) levels were quantified.
  • NK cell analysis was performed on RR-MS patients undergoing IFN-β treatment and those not receiving it.

Main Results:

  • NK cells from RR-MS patients on IFN-β therapy showed increased expression of activating receptors.
  • Interleukin-22 (IL-22) levels were elevated in RR-MS patients undergoing IFN-β treatment.
  • These findings suggest a shift towards a pro-inflammatory NK cell phenotype with IFN-β therapy.

Conclusions:

  • IFN-β therapy in RR-MS patients is associated with enhanced NK cell activating profiles.
  • Elevated IL-22 levels in conjunction with increased NK cell activation suggest a pro-inflammatory role.
  • IFN-β may modulate NK cells towards a pro-inflammatory state in RR-MS treatment.