Ratthé, Claude et Girard, Denis 
ORCID: https://orcid.org/0000-0002-3342-5027
(2004).
Interleukin-15 enhances human neutrophil phagocytosis by a Syk-dependent mechanism: importance of the IL-15Ralpha chain.
Journal of Leukocyte Biology
, vol. 76
, nº 1.
pp. 162-168.
DOI: 10.1189/jlb.0605298.
Résumé
Interleukin-15 (IL-15) is a cytokine that possesses interesting, potential therapeutic properties. However, based on several parameters including activation of neutrophils, it is also recognized as a proinflammatory cytokine. The mechanisms by which IL-15 activates human neutrophil functions are not fully understood. Although these cells express a functional IL-15 receptor (IL-15R) composed of IL-15R?, IL-2/15R? (CD122), and ?c (CD132) subunits, the role of each receptor component has not been investigated in IL-15-induced human neutrophil responses. In the present study, fluorescein-activated cell sorter analysis revealed that the ability of IL-15 to enhance neutrophil phagocytosis is not a result of increased expression of IL-15R?, CD122, or CD132 on the neutrophil cell surface. Pretreatment of neutrophils with specific antibodies to IL-15R?, CD122, or CD132 was found to inhibit phagocytosis of opsonized-sheep red blood cells by nearly 40%, 21%, and 27%, respectively. As expected, pretreatment of neutrophils with anti-IL-2R? (CD25) had no effect. Pretreatment of cells with the Syk inhibitor piceatannol was found to significantly inhibit the ability of IL-15 to enhance phagocytosis. In addition, IL-15 was found to induce tyrosine phosphorylation of Syk that was largely inhibited by pretreating cells with piceatannol. Moreover, we found that Syk kinase is physically associated with IL-15R?. We conclude ttiat IL-15R enhances nentrophil phagocytosis by a Syk-dependent mechanism and that the IL-15R? chain plays a key role in mediating this response, at least by interacting with Syk kinase.
| Type de document: | Article |
|---|---|
| Mots-clés libres: | - |
| Centre: | Centre INRS-Institut Armand Frappier |
| Date de dépôt: | 21 nov. 2024 20:20 |
| Dernière modification: | 21 nov. 2024 20:20 |
| URI: | https://espace.inrs.ca/id/eprint/15102 |
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