Abstract

There is established evidence that cytotoxic CD8+ T cells are important mediators of immunity against the bovine intracellular protozoan parasite T. parva. However, the mechanism by which the specific CD8+ T cells kill parasitized cells is not understood. Although the predominant pathway used by human and murine CD8+ T cells to kill pathogen-infected cells is granule exocytosis, involving release of perforin and granzyme B, there is to date a lack of published information on the biological activities of bovine granzyme B. The present study set out to define the functional activities of bovine granzyme B and determine its role in mediating killing of T. parva-parasitized cells. DNA constructs encoding functional and non-functional forms of bovine granzyme B were produced and the proteins expressed in Cos-7 cells were used to establish an enzymatic assay to detect and quantify expression of functional granzyme B protein. Using this assay, the levels of killing of different T. parva-specific CD8+ T cell clones were found to be significantly correlated with levels of granzyme B protein, but not mRNA transcript, expression. Experiments using inhibitors specific for perforin and granzyme B confirmed that CD8+ T cell killing of parasitized cells is dependent on granule exocytosis and specifically granzyme B. Further studies showed that granzyme B-mediated death of parasitized cells is independent of caspases, but involves activation of the pro-apoptotic molecule Bid.

Details

Title
Granzyme B is an essential mediator in CD8+ T cell killing of Theileria parva-infected cells
Author
Yang, Jie; Pemberton, Alan; Morrison, W Ivan; Connelley, Timothy K
University/institution
Cold Spring Harbor Laboratory Press
Section
New Results
Publication year
2018
Publication date
May 18, 2018
Publisher
Cold Spring Harbor Laboratory Press
Source type
Working Paper
Language of publication
English
ProQuest document ID
2071232845
Copyright
�� 2018. This article is published under https://creativecommons.org/publicdomain/zero/1.0/ (���the License���). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.