Interleukin 15 primes natural killer cells to kill via NKG2D and cPLA2 and this pathway is active in psoriatic arthritis.
Interleukin 15 primes natural killer cells to kill via NKG2D and cPLA2 and this pathway is active in psoriatic arthritis.
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DOI：
10.1371/journal.pone.0076292
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发表时间：
2013
期刊：
影响因子：
3.7
通讯作者：
Jabri B
中科院分区：
文献类型：
--
作者：
Tang F;Sally B;Ciszewski C;Abadie V;Curran SA;Groh V;Fitzgerald O;Winchester RJ;Jabri B
NK cells are large granular lymphocytes that form a critical component of the innate immune system, whose functions include the killing of cells expressing stress-induced molecules. It is increasingly accepted that despite being considered prototypical effector cells, NK cells require signals to reach their full cytotoxic potential. We previously showed that IL-15 is capable of arming CD8 effector T cells to kill independently of their TCR via NKG2D in a cPLA2-dependent process. As NK cells also express NKG2D, we wanted to investigate whether this pathway functioned in an analogous manner and if resting NK cells could be primed to the effector phase by IL-15. Furthermore, to establish relevance to human disease we studied a possible role for this pathway in the pathogenesis of psoriatic arthritis, since there are aspects of this disease that suggest a potential effector role for the innate immune system. We found that PsA patients had upregulated IL-15 and MIC in their affected synovial tissues, and that this unique inflammatory environment enabled NK cell activation and killing via NKG2D and cPLA2. Moreover, we were able to reproduce the phenotype of joint NK cells from blood NK cells by incubating them with IL-15. Altogether, these findings suggest a destructive role for NK cells when activated by environmental stress signals during the pathogenesis of PsA and demonstrate that IL-15 is capable of priming resting NK cells in tissues to the effector phase.
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DOI：
10.1084/jem.20081648
发表时间：
2009-04-13
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Dai Z;Turtle CJ;Booth GC;Riddell SR;Gooley TA;Stevens AM;Spies T;Groh V
通讯作者：
Groh V
DOI：
10.1126/science.1198687
发表时间：
2011-01-07
期刊：
Science (New York, N.Y.)
影响因子：
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作者：
Vivier E;Raulet DH;Moretta A;Caligiuri MA;Zitvogel L;Lanier LL;Yokoyama WM;Ugolini S
通讯作者：
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影响因子：
29.4
作者：
Allez, Matthieu;Tieng, Vannary;Toubert, Antoine
通讯作者：
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影响因子：
56.9
作者：
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通讯作者：
Spies, T
DOI：
10.4049/jimmunol.1002653
发表时间：
2011-02-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Bowness P;Ridley A;Shaw J;Chan AT;Wong-Baeza I;Fleming M;Cummings F;McMichael A;Kollnberger S
通讯作者：
Kollnberger S