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A Unique Lymphotoxin αβ-Dependent Pathway Regulates Thymic Emigration of Vαl4 Invariant Natural Killer T Cells

Ann Sophie Franki, Katrien Van Beneden, Pieter Dewint, Kirsten J. L. Hammond, Stijn Lambrecht, Georges Leclercq, Mitchell Kronenberg, Dieter Deforce and Dirk Elewaut
Proceedings of the National Academy of Sciences of the United States of America
Vol. 103, No. 24 (Jun. 13, 2006), pp. 9160-9165
Stable URL: http://www.jstor.org/stable/30051914
Page Count: 6
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
A Unique Lymphotoxin αβ-Dependent Pathway Regulates Thymic Emigration of Vαl4 Invariant Natural Killer T Cells
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Abstract

Natural killer (NK) T cells using an invariant Vαl4 (Vα14i) T cell receptor rearrangement form a distinct immunoregulatory T cell lineage. Several studies indicated that a NK1.1⁻ Vα14i NKT precursor cell differentiates and expands within the thymus before export to the peripheral tissues occurs. However, little is known about the signals that cause the emigration of Vα14i NKT cells from the thymus to the periphery. Here we show that signaling of lymphotoxin (LT) αβ through the LTβ receptor (LTβR) is indispens-able for regulating peripheral but not thymic Vα14i NKT cell numbers. Homing to and homeostatic proliferation of thymic Vα14i NKT cells in peripheral organs, however, was not dependent on LTβR. Instead, our data indicate that a LTβR-expressing thymic stromal cell regulates the thymic emigration of Vα14i NKT cells but not conventional T cell receptor αβ cells.

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