NDLI: Discontinued postnatal thymocyte development in sphingosine 1-phosphate-lyase-deficient mice.

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Discontinued postnatal thymocyte development in sphingosine 1-phosphate-lyase-deficient mice.

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Discontinued postnatal thymocyte development in sphingosine 1-phosphate-lyase-deficient mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Van Veldhoven, Paul P. Krueger, Andreas Bode, Constantin Münk, Anika Weber, Claudia Gräler, Markus H.
Description	Country affiliation: Germany Author Affiliation: Weber C ( Institute for Immunology, Hannover Medical School, Hanover 30625, Germany.)
Abstract	Circulation of lymphocytes through peripheral lymphoid tissues as well as progenitor entry into the thymus and its output of mature T cells are critical for normal immune function. Egress of lymphocytes from both peripheral lymphoid organs and thymus is dependent on sphingosine 1-phosphate (S1P) gradients. S1P-lyase 1 (SGPL1) deficiency leads to accumulation of S1P in lymphoid tissues, which blocks lymphocyte egress and induces thymus atrophy. In this study, we investigated thymocyte development in SGPL1-deficient mice (SGPL1(-/-)), which exhibited postnatal discontinuation of early thymocytopoiesis starting at 2 wk after birth. SGPL(-/-) thymi showed a loss of developing thymocytes in the thymic cortex between 2 and 4 wk of age, whereas mature thymocytes accumulated in the medulla. Detailed analysis demonstrated a deficit in thymic early T cell progenitors (ETP) as the principal reason for discontinued thymocyte development. This developmental block was accompanied by accumulation of ceramides, resulting in enhanced apoptosis of developing T cells. Lack of immigration or settlement of ETP completely halted thymocyte development. We conclude that increased ceramide levels in the thymus of SGPL1(-/-) mice abrogate thymic development postnatally by enhanced thymocyte apoptosis and depletion of thymic ETP. Our findings indicate that potentially therapeutic immunosuppression by SGPL1 inhibition should benefit from monitoring ceramides to prevent their increase to apoptosis- inducing levels.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	7
Volume Number	183
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2009-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Aldehyde-lyases Deficiency Genetics Animals, Newborn Immunology Cell Differentiation Thymus Gland Enzymology Antagonists & Inhibitors Animals Atrophy Cell Movement Ceramides Biosynthesis Physiology Lymphopenia Lymphopoiesis Mice Mice, Knockout Mice, Nude Stem Cells Pathology Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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