The Immune Memory Response of In Vitro-Polarised Th1, Th2, and Th17 Cells in the Face of Ovalbumin-Transgenic Leishmania major in a Mouse Model

Author:

Tedla Mebrahtu G.1ORCID,Nahar Musammat F.2,Every Alison L.3,Scheerlinck Jean-Pierre Y.4

Affiliation:

1. Department of Pediatrics, School of Medicine, University of Missouri-Columbia, Columbia, MO 65211, USA

2. Department of Health Science and Community, Swinburne University of Technology, Hawthorn, VIC 3122, Australia

3. Australian Academy of Technological Sciences and Engineering, Forrest, ACT 2603, Australia

4. Centre for Animal Biotechnology, Faculty of Veterinary and Agricultural Sciences, The University of Melbourne, Parkville, VIC 3010, Australia

Abstract

Th1 and Th2 cytokines determine the outcome of Leishmania major infection and immune protection depends mainly on memory T cells induced during vaccination. This largely hinges on the nature and type of memory T cells produced. In this study, transgenic Leishmania major strains expressing membrane-associated ovalbumin (mOVA) and soluble ovalbumin (sOVA) were used as a model to study whether fully differentiated Th1/Th2 and Th17 cells can recall immune memory and tolerate pathogen manipulation. Naïve OT-II T cells were polarised in vitro into Th1/Th2 cells, and these cells were transferred adoptively into recipient mice. Following the transferral of the memory cells, the recipient mice were challenged with OVA transgenic Leishmania major and a wild-type parasite was used a control. The in vitro-polarised T helper cells continued to produce the same cytokine signatures after being challenged by both forms of OVA-expressing Leishmania major parasites in vivo. This suggests that antigen-experienced cells remain the same or unaltered in the face of OVA-transgenic Leishmania major. Such ability of these antigen-experienced cells to remain resilient to manipulation by the parasite signifies that vaccines might be able to produce immune memory responses and defend against parasitic immune manipulation in order to protect the host from infection.

Publisher

MDPI AG

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