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
ISSN
2692-8205
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.