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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Immune surveillance is an integral part of the innate immune system, involving the continuous monitoring of peripheral tissues to detect and respond to pathogens, infected cells, or cancerous cells. This surveillance is conducted primarily by natural killer (NK) cells and phagocytes, which employ distinct but complementary mechanisms to identify and eliminate threats.
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Updated: Aug 14, 2025

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase G6PI-Induced RA Mice
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MicroRNAs Targeting Programmed Cell Death Protein 1 (PD-1) Promote Natural Killer Cell Exhaustion in Rheumatoid

Maryam Hemmatzadeh1, Elham Ahangar Parvin2, Alireza Ghanavatinejad3

  • 1Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran AND Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran AND Department of Immunology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. m.hematzadeh1991@gmail.com.

Iranian Journal of Allergy, Asthma, and Immunology
|January 14, 2023
PubMed
Summary

In rheumatoid arthritis (RA), natural killer (NK) cells show exhaustion, indicated by higher programmed cell death protein 1 (PD-1) levels. MicroRNAs (miRNAs) like miR-28, miR-138, and miR-4717 may regulate this exhaustion in RA patients.

Keywords:
MicroRNANK cell exhaustionNatural killer cellProgrammed cell death protein 1Rheumatoid arthritis

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Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Natural killer (NK) cells are implicated in rheumatoid arthritis (RA) pathogenesis.
  • NK cell exhaustion, marked by programmed cell death protein 1 (PD-1) upregulation, is observed in RA.
  • MicroRNAs (miRNAs) are potential regulators of PD-1 expression on NK cells.

Purpose of the Study:

  • To investigate PD-1 expression on NK cells in RA patients.
  • To explore the role of miRNAs in modulating PD-1 expression in RA-associated NK cell exhaustion.

Main Methods:

  • Flow cytometry was used to analyze PD-1 expression on NK cells.
  • Real-time PCR quantified PD-1 mRNA and miRNA levels in isolated NK cells from 40 RA patients and 20 healthy controls.

Main Results:

  • RA patients exhibited significantly higher frequencies and mean fluorescence intensity (MFI) of PD-1-expressing NK cells compared to healthy subjects.
  • PD-1 mRNA levels were significantly upregulated in NK cells from RA patients.
  • Expression of miR-28, miR-138, and miR-4717 was significantly downregulated in NK cells from RA patients.

Conclusions:

  • NK cell exhaustion, characterized by increased PD-1 expression, is a feature of RA.
  • Downregulation of specific miRNAs (miR-28, miR-138, miR-4717) in NK cells may contribute to PD-1 upregulation and exhaustion in RA.
  • These findings suggest a regulatory role for miRNAs in NK cell exhaustion within the context of rheumatoid arthritis.