Abstract

Circulating γδ T cells in healthy individuals rapidly respond to bacterial and viral pathogens. Many studies have demonstrated that γδ T cells are activated and expanded by Listeria monocytogenes (L.monocytogenes), a foodborne bacterial pathogen with high fatality rates. However, the roles of γδ T cells during L.monocytogenes infection are not clear. In the present study, we characterized the morphological characteristics of phagocytosis in γδ T cells after L.monocytogenes infection using transmission electron microscopy. Results show activation markers including HLA-DR and lymph node-homing receptor CCR7 on γδ T cells were upregulated after stimulation via L.monocytogenes. Significant proliferation and differentiation of primary αβ T cells was also observed after co-culture of peripheral blood mononuclear cells with γδ T cells anteriorly stimulated by L.monocytogenes. L.monocytogenes infection decreased the percentage of γδ T cells in mouse IELs and increased MHC-II expression on the surface of γδ T cells in vivo. Our findings shed light on antigen presentation of γδ T cells during L.monocytogenes infection.

Highlights

  • Human γδ T cells are a subset ofT cells with a T cell receptor (TCR) ­composed of γ and δ chains [1]

  • We first assessed the phagocytic capacity of γδ T cells. γδ T cells were expanded by culturing Peripheral blood mononuclear cells (PBMCs) in antipan-TCRγδ mAb-coated plates with RPMI 1640 medium containing IL-2 for 10 d

  • The results show that the ratios of αβ T cells (Figure 5B), CD4 + T cells (­Figure 5C) and CD8 + T cells (Figure 5D) significantly increased when cocultured with L. ­monocytogenes-infected-γδ T cells

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Summary

Introduction

T cells with a T cell receptor (TCR) ­composed of γ and δ chains [1]. They constitute a small proportion (3~10%) of circulating CD3+ T-lymphocytes in peripheral blood. Compared with αβ T cells, γδ T cells recognize antigens without major histocompatibility complex (MHC) restriction and without help from antigen presenting cells (APC). They directly bind to stress-­ induced ligands such as heat shock proteins and mutS homolog 2 (hMSH2) [2,3,4].

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