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Related Concept Videos

Cells of the Innate Immune Response01:28

Cells of the Innate Immune Response

The innate immune response is an immediate and non-specific response against pathogens, acting swiftly to prevent the spread of infections. The primary cells involved in this response are phagocytes and natural killer (NK) cells.
Phagocytes
Phagocytes police the peripheral tissues by removing cellular debris and responding to the invasion of foreign substances or pathogens. Many phagocytes attack and remove microorganisms even before lymphocytes detect them. The human body has two general...

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Related Experiment Video

Updated: Jul 11, 2026

Adoptive Immunotherapy of iNKT Cells in Glucose-6-Phosphate Isomerase (G6PI)-Induced RA Mice
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NKG2A inhibits TH2 cell effector function in vitro.

Robert J Freishtat1, Bahar Mojgani, Maryam Nazemzadeh

  • 1Division of Emergency Medicine, Children's National Medical Center, Washington, DC, USA. rfreishtat@cnmcresearch.org

BMC Pulmonary Medicine
|October 12, 2007
PubMed
Summary
This summary is machine-generated.

Signaling through NKG2A inhibits T helper 2 (TH2) cell function, indicated by reduced IL-4 production. This finding suggests NKG2A agonists could modulate Th1/Th2 balance in Th2-dominant diseases.

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In Vitro Functional Analysis of Regulatory T cells: Focus On Proliferation And Differentiation
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In Vitro Functional Analysis of Regulatory T cells: Focus On Proliferation And Differentiation

Published on: June 9, 2026

Area of Science:

  • Immunology
  • Cellular Immunology
  • T cell differentiation

Background:

  • NKG2A, an inhibitory receptor, binds HLA-E and is expressed on activated TH2 cells.
  • Previous work established NKG2A expression on TH2 but not TH1 cells.

Purpose of the Study:

  • To investigate the functional impact of NKG2A signaling on human ex vivo TH2 cells.
  • To measure cytokine production in TH2 cells stimulated with an NKG2A-specific agonist.

Main Methods:

  • Human TH2 cells were purified and activated using anti-CD3/28 antibodies.
  • Cells were challenged with an NKG2A-specific agonist, and IL-4 production was measured via flow cytometry.

Main Results:

  • Activation increased NKG2A expression on TH2 cells (7.3% to 13.7%, p=0.03).
  • NKG2A agonist stimulation significantly reduced intracellular IL-4 expression in activated TH2 cells (25.5% to 9.3%, p=0.001).
  • NKG2A agonist did not alter NKG2A expression levels.

Conclusions:

  • NKG2A signaling suppresses TH2 effector function, specifically IL-4 production.
  • Targeting NKG2A may offer a therapeutic strategy for diseases characterized by Th2 cytokine dominance.