PDGF-D-PDGFRß signaling enhances IL-15-mediated human natural killer cell survival.
Proc Natl Acad Sci U S A
; 119(3)2022 01 18.
Article
em En
| MEDLINE
| ID: mdl-35027451
ABSTRACT
The axis of platelet-derived growth factor (PDGF) and PDGF receptor-beta (PDGFRß) plays prominent roles in cell growth and motility. In addition, PDGF-D enhances human natural killer (NK) cell effector functions when binding to the NKp44 receptor. Here, we report an additional but previously unknown role of PDGF-D, whereby it mediates interleukin-15 (IL-15)-induced human NK cell survival but not effector functions via its binding to PDGFRß but independent of its binding to NKp44. Resting NK cells express no PDGFRß and only a low level of PDGF-D, but both are significantly up-regulated by IL-15, via the nuclear factor κB signaling pathway, to promote cell survival in an autocrine manner. Both ectopic and IL-15-induced expression of PDGFRß improves NK cell survival in response to treatment with PDGF-D. Our results suggest that the PDGF-D-PDGFRß signaling pathway is a mechanism by which IL-15 selectively regulates the survival of human NK cells without modulating their effector functions.
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Base de dados:
MEDLINE
Assunto principal:
Fator de Crescimento Derivado de Plaquetas
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Células Matadoras Naturais
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Transdução de Sinais
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Interleucina-15
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Receptor beta de Fator de Crescimento Derivado de Plaquetas
Idioma:
En
Ano de publicação:
2022
Tipo de documento:
Article