Activation of the FcgammaReceptorIIIa on human natural killer cells leads to increased expression of functional interleukin-21 receptor-Reference-Cited by-同舟云学术

Activation of the FcgammaReceptorIIIa on human natural killer cells leads to increased expression of functional interleukin-21 receptor

Published:2017-05-04 Issue:5 Volume:6 Page:e1312045
ISSN:2162-402X
Container-title:OncoImmunology
language:en
Short-container-title:OncoImmunology

Author:

McMichael Elizabeth L.¹,Courtney Nicholas B.²,Duggan Megan C.¹,Wesolowski Robert³,Quiroga Dionisia³,Kondadasula Sri Vidya²,Atwal Lakhvir S.²,Bhave Neela²,Luedke Eric⁴,Jaime-Ramirez Alena Cristina⁵,Campbell Amanda R.¹⁶,Mo Xiaokui⁷,Byrd John C.⁸,Carson William E.¹⁴⁹

Affiliation:

1. Biomedical Sciences Graduate Program, College of Medicine, Columbus, OH, US

2. Comprehensive Cancer Center, Columbus, OH, USA

3. Division of Medical Oncology, Department of Internal Medicine, Columbus, OH, USA

4. Department of Surgery, Division of Surgical Oncology, Columbus, OH, USA

5. Department of Neurosurgery, Columbus, OH, USA

6. Medical Scientist Training Program, College of Medicine, Columbus, OH, USA

7. Center for Biostatistics, Columbus, OH, USA

8. Division of Hematology, Department of Internal Medicine, Columbus, OH, USA

9. Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, OH, USA

Publisher

Informa UK Limited

Subject

Oncology,Immunology,Immunology and Allergy

Link

https://www.tandfonline.com/doi/pdf/10.1080/2162402X.2017.1312045

Reference51 articles.

1. Interleukin (IL) 15 is a novel cytokine that activates human natural killer cells via components of the IL-2 receptor.

2. The functional characterization of interleukin-10 receptor expression on human natural killer cells

3. Human natural killer cells produce abundant macrophage inflammatory protein-1 alpha in response to monocyte-derived cytokines.

4. Stimulated natural killer cells secrete factors with chemotactic activity, including NAP-1/IL-8, which supports VLA-4- and VLA-5-mediated migration of T lymphocytes

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