کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5667810 1592268 2017 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Contribution of inhibitory receptor TIGIT to NK cell education
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Contribution of inhibitory receptor TIGIT to NK cell education
چکیده انگلیسی


- Inhibitory receptor TIGIT enhances NK cell effector function towards various stimuli.
- TIGIT+ NK cells from CD155-deficient hosts are rendered hypo-responsive.
- TIGIT contributes to NK cell education in an MHC-I-independent and CD226-unrelated manner.

Engagement of inhibitory receptors by cognate host MHC-I molecules triggers NK cell education, resulting in functional maturation and allowing NK cells to sense missing-self. However, NK cells also express inhibitory receptors for non-MHC-I ligands and their role in NK cell education is poorly understood. TIGIT is a recently identified inhibitory receptor that recognizes a non-MHC-I ligand CD155. Here, we demonstrated that TIGIT+ NK cells from wild-type mice exerted augmented responsiveness to various stimuli, including targets that lacked expression of CD155 ligand. TIGIT+ NK cells derived from CD155-deficient hosts, however, exhibited functional impairment, indicating that the engagement of TIGIT receptor by host CD155 promoted NK cell functional maturation. Furthermore, TIGIT deficiency impaired NK cell-mediated missing-self recognition and rejection of CD155- targets, such as allogenic splenocytes and certain tumor cells, in an MHC-I-independent and CD226-unrelated manner. Thus, TIGIT-CD155 pathway is also involved in the acquisition of optimal NK cell effector function, representing a novel MHC-I-independent education mechanism for NK cell tolerance and activation.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Autoimmunity - Volume 81, July 2017, Pages 1-12
نویسندگان
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