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Interferon-γ Receptor Signaling in Dendritic Cells Restrains Spontaneous Proliferation of CD4 T Cells in Chronic Lymphopenic Mice.
Knop, Laura Frommer, Charlotte Stoycheva, Diana Deiser, Katrin Blankenstein, Thomas Kammertoens, Thomas Dunay, Ildiko Rita Schüler, Thomas
Knop, Laura
Frommer, Charlotte
Stoycheva, Diana
Deiser, Katrin
Blankenstein, Thomas
Kammertoens, Thomas
Dunay, Ildiko Rita
Schüler, Thomas
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2019-01-01
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Abstract
In lymphopenic mice, T cells become activated and undergo lymphopenia-induced proliferation (LIP). However, not all T cells are equally sensitive to lymphopenia. Several lymphopenia-insensitive T cell clones were described and their non-responsiveness was mainly attributed to clone-specific properties. Here, we provide evidence for an additional, host-dependent mechanism restraining LIP of lymphopenia-insensitive CD4+ T cells. We show that such cells undergo LIP in lymphopenic mice lacking IFN-γ receptor (IFN-γR) expression, a process, which is promoted by the autocrine action of T cell-derived IFN-γ. Additionally, LIP of lymphopenia-insensitive CD4+ T cells requires an intact microflora and is accompanied by the massive accumulation of IL-6 and dendritic cells (DCs). Consistent with these results, IL-6 neutralization and the DC-specific restoration of IFN-γR expression are both sufficient to restrict LIP. Hence, the insensitivity of CD4+ T cells to lymphopenia relies on cell-intrinsic properties and a complex interplay between the commensal microflora, IL-6, IFN-γR+ DCs, and T cell-derived IFN-γ.
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Front Immunol. 2019 Feb 7;10:140. doi: 10.3389/fimmu.2019.00140. eCollection 2019.
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en
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1664-3224
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Attribution-NonCommercial-ShareAlike 4.0 International