Abstract
Within lymphopenic recipients, naïve T cells undergo proliferation that is induced by homeostatic mechanisms. Earlier studies have demonstrated that commensal antigens play a key role in inducing the proliferation. However, a relative contribution of endogenous self antigens in this process has not been formally investigated. In this study, we utilized a pharmacologic inhibitor that blocks T cell egress from the lymphoid tissues, antibiotics, and germ-free animals to examine the role of commensal and self antigens. The results suggest that T cell proliferation under lymphopenic conditions is a heterogeneous process triggered by both exogenous commensal and endogenous self antigens.
Copyright © 2011 Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, N.I.H., Intramural
MeSH terms
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Animals
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Autoantigens / immunology*
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Cell Proliferation / drug effects
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Fingolimod Hydrochloride
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Homeostasis / drug effects
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Homeostasis / immunology
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Immunologic Memory / drug effects
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Immunologic Memory / immunology
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Lymph Nodes / drug effects
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Lymph Nodes / immunology
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Lymphocyte Activation / drug effects
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Lymphocyte Activation / immunology
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Lymphopenia / immunology*
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Mice
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Mice, Inbred C57BL
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Propylene Glycols / pharmacology
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Receptors, Antigen, T-Cell / immunology
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Sphingosine / analogs & derivatives
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Sphingosine / pharmacology
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Spleen / drug effects
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Spleen / immunology
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T-Lymphocytes / drug effects
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T-Lymphocytes / immunology*
Substances
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Autoantigens
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Propylene Glycols
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Receptors, Antigen, T-Cell
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Fingolimod Hydrochloride
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Sphingosine