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Journal Articles International Journal of Molecular Sciences Year : 2021

Natural Killer Cells from Allergic Donors Are Defective in Their Response to CCL18 Chemokine

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1
Latiffa Amniai
  • Function : Author
Coline Ple
  • Function : Author
Mathieu Barrier
  • Function : Author
Patricia de Nadai
  • Function : Author
Philippe Marquillies
  • Function : Author
Han Vorng
  • Function : Author
Cécile Chenivesse
  • Function : Author
Anne Tsicopoulos

Abstract

Natural killer (NK) cells were originally described as cytolytic effector cells, but since then have been recognized to possess regulatory functions on immune responses. Chemokines locate NK cells throughout the body in homeostatic and pathological conditions. They may also directly stimulate immune cells. CCL18 is a constitutive and inducible chemokine involved in allergic diseases. The aim of this study was to evaluate CCL18’s effect on NK cells from allergic and nonallergic donors in terms of both chemotactic and immune effects. Results showed that CCL18 was able to induce migration of NK cells from nonallergic donors in a G-protein-dependent manner, suggesting the involvement of a classical chemokine receptor from the family of seven-transmembrane domain G-protein-coupled receptors. In contrast, NK cells from allergic patients were unresponsive. Similarly, CCL18 was able to induce NK cell cytotoxicity only in nonallergic subjects. Purified NK cells did not express CCR8, one of the receptors described to be involved in CCL18 functions. Finally, the defect in CCL18 response by NK cells from allergic patients was unrelated to a defect in CCL18 binding to NK cells. Overall, our results suggest that some NK cell functions may be defective in allergic diseases.

Dates and versions

hal-03654480 , version 1 (28-04-2022)

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Latiffa Amniai, Coline Ple, Mathieu Barrier, Patricia de Nadai, Philippe Marquillies, et al.. Natural Killer Cells from Allergic Donors Are Defective in Their Response to CCL18 Chemokine. International Journal of Molecular Sciences, 2021, 22 (8), pp.3879. ⟨10.3390/ijms22083879⟩. ⟨hal-03654480⟩
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