Abstract
The cross talk between NK cells and macrophages is emerging as a major line of defense against microbial infections and tumors. This study reveals a complex network of soluble mediators and cell-to-cell interactions allowing human classically activated (M1) macrophages, but not resting (M0) or alternatively activated (M2) macrophages, to prime resting autologous NK cells. In this article, we show that M1 increase NK cell cytotoxicity by IL-23 and IFN-β-dependent upregulation of NKG2D, IL-1b-dependent upregulation of NKp44, and trans-presentation of IL-15. Moreover, both IFN-β-dependent cis-presentation of IL-15 on NK cells and engagement of the 2B4-CD48 pathway are used by M1 to trigger NK cell production of IFN-γ. The disclosure of these synergic cellular mechanisms regulating the M1-NK cell cross talk provides novel insights to better understand the role of innate immune responses in the physiopathology of tumor biology and microbial infections.
| Original language | English |
|---|---|
| Pages (from-to) | 2818-2828 |
| Number of pages | 11 |
| Journal | Journal of Immunology |
| Volume | 195 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Sep 15 2015 |
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ASJC Scopus subject areas
- Immunology
- Medicine(all)
Cite this
Priming of human resting NK cells by autologous M1 macrophages via the engagement of IL-1b, IFN-β, and IL-15 pathways. / Mattiola, Irene; Pesant, Matthieu; Tentorio, Paolo F.; Molgora, Martina; Marcenaro, Emanuela; Lugli, Enrico; Locati, Massimo; Mavilio, Domenico.
In: Journal of Immunology, Vol. 195, No. 6, 15.09.2015, p. 2818-2828.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Priming of human resting NK cells by autologous M1 macrophages via the engagement of IL-1b, IFN-β, and IL-15 pathways
AU - Mattiola, Irene
AU - Pesant, Matthieu
AU - Tentorio, Paolo F.
AU - Molgora, Martina
AU - Marcenaro, Emanuela
AU - Lugli, Enrico
AU - Locati, Massimo
AU - Mavilio, Domenico
PY - 2015/9/15
Y1 - 2015/9/15
N2 - The cross talk between NK cells and macrophages is emerging as a major line of defense against microbial infections and tumors. This study reveals a complex network of soluble mediators and cell-to-cell interactions allowing human classically activated (M1) macrophages, but not resting (M0) or alternatively activated (M2) macrophages, to prime resting autologous NK cells. In this article, we show that M1 increase NK cell cytotoxicity by IL-23 and IFN-β-dependent upregulation of NKG2D, IL-1b-dependent upregulation of NKp44, and trans-presentation of IL-15. Moreover, both IFN-β-dependent cis-presentation of IL-15 on NK cells and engagement of the 2B4-CD48 pathway are used by M1 to trigger NK cell production of IFN-γ. The disclosure of these synergic cellular mechanisms regulating the M1-NK cell cross talk provides novel insights to better understand the role of innate immune responses in the physiopathology of tumor biology and microbial infections.
AB - The cross talk between NK cells and macrophages is emerging as a major line of defense against microbial infections and tumors. This study reveals a complex network of soluble mediators and cell-to-cell interactions allowing human classically activated (M1) macrophages, but not resting (M0) or alternatively activated (M2) macrophages, to prime resting autologous NK cells. In this article, we show that M1 increase NK cell cytotoxicity by IL-23 and IFN-β-dependent upregulation of NKG2D, IL-1b-dependent upregulation of NKp44, and trans-presentation of IL-15. Moreover, both IFN-β-dependent cis-presentation of IL-15 on NK cells and engagement of the 2B4-CD48 pathway are used by M1 to trigger NK cell production of IFN-γ. The disclosure of these synergic cellular mechanisms regulating the M1-NK cell cross talk provides novel insights to better understand the role of innate immune responses in the physiopathology of tumor biology and microbial infections.
UR - http://www.scopus.com/inward/record.url?scp=84941790490&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84941790490&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.1500325
DO - 10.4049/jimmunol.1500325
M3 - Article
C2 - 26276870
AN - SCOPUS:84941790490
VL - 195
SP - 2818
EP - 2828
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 6
ER -