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Novel cooperation between CX 3 CL 1 and CCL 26 inducing NK cell chemotaxis via CX 3 CR 1: a possible mechanism for NK cell infiltration of the allergic nasal tissue
Author(s) -
ElShazly A. E.,
Doloriert H. C.,
Bisig B.,
Lefebvre P. P.,
Delvenne P.,
Jacobs N.
Publication year - 2013
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/cea.12022
Subject(s) - chemokine , chemotaxis , flow cytometry , chemistry , microbiology and biotechnology , immunology , eotaxin , allergic inflammation , receptor , inflammation , biology , biochemistry
Summary Background Recent data indicated that natural killer ( NK ) cells and chemokines could play a pivotal role in nasal inflammation. CX 3 CR 1, the only receptor for fractalkine/ CX 3 CL 1, is abundantly expressed by NK cells, and was recently shown to also be a receptor for eotaxin‐3/ CCL 26. However, no reports explored the NK cells‐ CX 3 CL 1‐ CCL 26 axis via CX 3 CR 1 in allergy. Objective Our goals were first to determine specifically NK cell recruitment pattern in nasal tissue of allergic chronic rhinosinusitis ( ACRS ) and non‐allergic chronic rhinosinusitis ( NACRS ) patients in comparison with healthy controls, and secondly, to investigate the function of CX 3 CR 1 in NK cell migration. Methods Immunohistochemistry, microchemotaxis chambers, flow cytometry and confocal microscopy were used in this study. Results Herein, we showed that NK cells infiltrated the epithelial layers of nasal tissue only in ACRS patients and not in NACRS patients or controls. NK cells were also more numerous in the stroma of the nasal tissue from ACRS patients compared with NACRS patients or controls. This migration could be mediated by both CX3CL1 and CCL 26, as these two chemokines induced NK cell migration. Moreover, both molecules also stimulated cytoskeleton changes and F‐actin reorganisation in NK cells. Chemotaxis and cytoskeleton changes were sensitive to genistein, a tyrosine kinase inhibitor. By flow cytometry, we demonstrated that a single antigen nasal provocation challenge increased the expression of CX 3 CR 1 on NK cells in allergic rhinitis ( AR ) patients. The function of this receptor was associated with a significant augmentation of NK cell chemotaxis against the optimal doses of CX 3 CL 1 and CCL 26. Conclusions and Clinical Relevance Our results highlight a novel role for CX 3 CR 1 in NK cell migration that may contribute to the NK cell trafficking to the allergic upper airway. This could be mediated largely by CX 3 CL 1 and CCL 26 stimulation of the tyrosine kinase pathway.