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Updated: Jan 30, 2026

Expansion, Purification, and Functional Assessment of Human Peripheral Blood NK Cells
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Siglec-7 on peripheral blood eosinophils: Surface expression and function.

Fanny Legrand1, Nadine Landolina2, Ilan Zaffran2

  • 1Human Eosinophil Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland.

Allergy
|January 29, 2019
PubMed
Summary
This summary is machine-generated.

Siglec-7 is present on human eosinophils and inhibits their activation. Targeting Siglec-7 may improve treatments for eosinophil disorders, but inhibition could worsen inflammation.

Keywords:
ITIMSiglec-7Siglec-8apoptosiseosinophiliaeosinophilshypereosinophilic syndromesignaling

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Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Siglec-7 is an inhibitory receptor on human eosinophils.
  • Its role in eosinophil function is largely unknown compared to other inhibitory receptors.

Purpose of the Study:

  • To investigate Siglec-7 expression and function in eosinophils from normal and eosinophilic donors.
  • To understand Siglec-7's impact on eosinophil activation and signaling pathways.

Main Methods:

  • Quantified Siglec-7 expression using flow cytometry and qPCR.
  • Measured soluble Siglec-7 (sSiglec-7) levels via ELISA.
  • Assessed Siglec-7's effect on eosinophil viability and degranulation in vitro.
  • Studied signal transduction pathways using Western blot.

Main Results:

  • Siglec-7 expressed on eosinophils from all donors; surface expression correlated with absolute eosinophil count (AEC).
  • Siglec-7 expression increased on eosinophils stimulated with GM-CSF or IL-5.
  • Cross-linking Siglec-7 inhibited GM-CSF-induced mediator release and modulated SHP-1 and ERK1/2/p38 phosphorylation, but did not induce apoptosis.

Conclusions:

  • Siglec-7 is constitutively expressed on human eosinophils and downmodulates their activation.
  • Targeting Siglec-7 could enhance treatment efficacy in eosinophil-driven diseases.
  • Inhibiting Siglec-7 might promote eosinophilic inflammation, suggesting caution in therapeutic strategies.