Thy-1 stimulation of mouse T cells induces a delayed T cell receptor-like signal that results in Ca2+‑independent cytotoxicity

  • Authors:
    • Suzanne Furlong
    • Melanie R. Power Coombs
    • David W. Hoskin
  • View Affiliations

  • Published online on: August 14, 2017     https://doi.org/10.3892/mmr.2017.7242
  • Pages: 5683-5692
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Abstract

Antibody-mediated crosslinking of Thy-1 [also known as cluster of differentiation (CD)90], results in a T cell receptor (TcR)‑like signal; however, the impact of Thy‑1 stimulation in comparison to TcR stimulation on T cell activation and effector function has yet to be fully elucidated. In the present study, the outcome of Thy‑1‑ and TcR‑induced stimulation of T cells was investigated in mice, using fragment crystalizable (Fc) receptor‑bound antibodies and costimulatory signals provided by syngeneic lipopolysaccharide‑matured bone marrow‑derived dendritic cells. Compared with TcR signaling, Thy‑1 signaling initiated a less robust proliferative response in T cells, as determined by tritiated‑thymidine incorporation. In addition, enzyme‑linked immunosorbent assays revealed that interleukin‑2 production was reduced, and the expression of CD25 and cyclin D3 was weaker in Thy‑1‑stimulated cells, as determined by western blotting; however, the expression of cyclin‑dependent kinase 6 was similar to that in TcR‑induced T cells. Furthermore, western blotting demonstrated that the phosphorylation of ζ-chain‑associated protein kinase 70 and extracellular signal‑regulated kinase 1/2 was delayed following Thy‑1 stimulation. DNA fragmentation assays revealed that cytotoxic effector function was also slower to develop in Thy‑1‑stimulated T cells, required more time to be effective and was largely Ca2+‑independent; these findings suggested that Fas ligand rather than granule‑associated perforin was involved in T cell effector function. In conclusion, the present results suggested that Thy‑1 signaling may contribute to the regulation of T cell homeostasis and the development of non‑specific T cell‑mediated cytotoxicity. However, further studies are required to elucidate the exact physiological roles of TcR‑like signals that result from Thy‑1 crosslinking and to investigate the molecular mechanisms that are involved.

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October-2017
Volume 16 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Furlong S, Power Coombs MR and Hoskin DW: Thy-1 stimulation of mouse T cells induces a delayed T cell receptor-like signal that results in Ca2+‑independent cytotoxicity. Mol Med Rep 16: 5683-5692, 2017
APA
Furlong, S., Power Coombs, M.R., & Hoskin, D.W. (2017). Thy-1 stimulation of mouse T cells induces a delayed T cell receptor-like signal that results in Ca2+‑independent cytotoxicity. Molecular Medicine Reports, 16, 5683-5692. https://doi.org/10.3892/mmr.2017.7242
MLA
Furlong, S., Power Coombs, M. R., Hoskin, D. W."Thy-1 stimulation of mouse T cells induces a delayed T cell receptor-like signal that results in Ca2+‑independent cytotoxicity". Molecular Medicine Reports 16.4 (2017): 5683-5692.
Chicago
Furlong, S., Power Coombs, M. R., Hoskin, D. W."Thy-1 stimulation of mouse T cells induces a delayed T cell receptor-like signal that results in Ca2+‑independent cytotoxicity". Molecular Medicine Reports 16, no. 4 (2017): 5683-5692. https://doi.org/10.3892/mmr.2017.7242