TLR-Stimulated Neutrophils Instruct NK Cells To Trigger Dendritic Cell Maturation and Promote Adaptive T Cell Responses
Artikel i vetenskaplig tidskrift, 2015

Polymorphonuclear neutrophils (PMNs) are innate effector cells with pivotal roles in pathogen recognition, phagocytosis, and eradication. However, their role in the development of subsequent immune responses is incompletely understood. This study aimed to identify mechanisms of relevance to the cross talk between human neutrophils and NK cells and its potential role in promoting adaptive immunity. TLR-stimulated PMNs were found to release soluble mediators to attract and activate NK cells in vitro. PMN-conditioned NK cells displayed enhanced cytotoxicity and cytokine production, and responded vigorously to ensuing stimulation with exogenous and endogenous IL-12. The neutrophil-induced activation of NK cells was prevented by caspase-1 inhibitors and by natural antagonists to IL-1 and IL-18, suggesting a role for the NOD-like receptor family pyrin domain containing-3 inflammasome. In addition, PMN-conditioned NK cells triggered the maturation of monocyte-derived dendritic cells, which promoted T cell proliferation and IFN-gamma production. These data imply that neutrophils attract NK cells to sites of infection to convert these cells into an active state, which drives adaptive immune responses via maturation of dendritic cells. Our results add to a growing body of evidence that suggests a sophisticated role for neutrophils in orchestrating the immune response to pathogens.

RECEPTOR

NATURAL-KILLER-CELLS

LYMPHOCYTES

APOPTOSIS

INFLAMMASOME

Immunology

INNATE

DEATH

RELEASE

IMMUNITY

ACTIVATION

Författare

Rebecca E Riise

Göteborgs universitet

Elin Bernson

Göteborgs universitet

Johan Aurelius

Göteborgs universitet

Anna Martner

Göteborgs universitet

S. Pesce

M. Della Chiesa

E. Marcenaro

Johan Bylund

Göteborgs universitet

Kristoffer Hellstrand

Göteborgs universitet

L. Moretta

A. Moretta

Fredrik B Thorén

Göteborgs universitet

Journal of Immunology

0022-1767 (ISSN) 1550-6606 (eISSN)

Vol. 195 3 1121-1128

Ämneskategorier

Immunologi inom det medicinska området

DOI

10.4049/jimmunol.1500709

PubMed

26085684