Asset Details
Do you wish to reserve the book?
Involvement of NK 1.1–Positive γδT Cells in Interleukin-18 Plus Interleukin-2–Induced Interstitial Lung Disease
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Involvement of NK 1.1–Positive γδT Cells in Interleukin-18 Plus Interleukin-2–Induced Interstitial Lung Disease
Do you wish to request the book?
Involvement of NK 1.1–Positive γδT Cells in Interleukin-18 Plus Interleukin-2–Induced Interstitial Lung Disease
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Involvement of NK 1.1–Positive γδT Cells in Interleukin-18 Plus Interleukin-2–Induced Interstitial Lung Disease
2011
Overview
Interstitial lung disease (ILD) is induced by various factors in humans. However, the exact mechanism of ILD remains elusive. This study sought to determine the role of natural killer (NK) 1.1+ γδT cells in ILD. The injection of IL-18 plus IL-2 (IL-18/IL-2) into C57BL6 (B6) mice induced acute ILD that resembled early-stage human ILD. An accumulation of NK1.1+ γδT cells similar to NK cells was evident in the lungs. The T Cell Receptor (TCR) Vγ and Vδ repertoires of NK1.1+ γδT cells indicated polyclonal expansion. The expression of IL-2 receptor β (Rβ) and IL-18Rβ in NK1.1+ γδT cells was higher than in NK1.1− γδT cells. IL-18/IL-2 stimulated the proliferation of NK1.1+ γδT cells, but not NK1.1− γδT cells. The IL-18/IL-2–stimulated NK1.1+ γδT cells produced higher concentrations of IFN-γ than did NK1.1− γδT cells. Moreover, NK1.1+ γδT and NK1.1− γδT cells constituted completely different cell populations. The IL-18/IL-2–induced ILD was milder in TCRδ−/− and IFN-γ−/− mice, compared with B6 mice. Furthermore, cell-transfer experiments demonstrated that NK1.1+ γδT cells could induce the expansion of NK cells and IFN-γ mRNA in the lung by IL-18/IL-2. Our results suggest that NK1.1+ γδT cells function as inflammatory mediators in the early phase of IL-18/IL-2–induced ILD.
Publisher
Oxford University Press
Subject
/ Female
/ Humans
/ Interferon-gamma - metabolism
/ Killer Cells, Natural - cytology
/ Lung Diseases, Interstitial - metabolism
/ Mice
/ mRNA
/ NK Cell Lectin-Like Receptor Subfamily B - biosynthesis
/ NK Cell Lectin-Like Receptor Subfamily B - genetics
/ Receptors, Antigen, T-Cell, gamma-delta - metabolism
