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

Int J Mol Sci

U1019-UMR 9017-CIIL-Center for Infection and Immunity of Lille, Institut Pasteur de Lille, University of Lille, CNRS, Inserm, CHU Lille, F-59000 Lille, France.

Published: April 2021

AI Article Synopsis

  • * The study focused on CCL18, a chemokine linked to allergic diseases, revealing that it effectively stimulates NK cell migration and cytotoxicity in nonallergic individuals but not in those with allergies.
  • * NK cells from allergic patients did not respond to CCL18, indicating a potential defect in their immune functions, while the inability to respond was not due to a problem with CCL18 binding.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8068884PMC
http://dx.doi.org/10.3390/ijms22083879DOI Listing

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