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Thymic Medullary Epithelial Cell Differentiation Thymocyte Emigrtion, and Control of Autoimmunity Require Lympho-Epithelial Cross Talk via LTβR

MPG-Autoren
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Boehm,  Thomas
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Bleul,  Conrad C.
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Zitation

Boehm, T., Scheu, S., Pfeffer, K., & Bleul, C. C. (2003). Thymic Medullary Epithelial Cell Differentiation Thymocyte Emigrtion, and Control of Autoimmunity Require Lympho-Epithelial Cross Talk via LTβR. Journal of Experimental Medicine, 198(5), 757-769.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-002B-94FF-7
Zusammenfassung
Thymocytes depend on the interaction with thymic epithelial cells for the generation of a diverse, nonautoreactive T cell repertoire. In turn, thymic epithelial cells acquire their three-dimensional cellular organization via instructive signals from developing thymocytes. The nature of these signals has been elusive so far. We show that thymocytes and medullary epithelial cells (MECs) communicate via the lymphotoxin β receptor (LTβR) signaling axis. Normal differentiation of thymic MECs requires LTβR ligand on thymocytes and LTβR together with nuclear factor-κB-inducing kinase (Nik) in thymic epithelial cells. Impaired lympho-epithelial cross talk in the absence of the LTβR causes aberrant differentiation and reduced numbers of thymic MECs, leads to the retention of mature T lymphocytes, and is associated with autoimmune phenomena, suggesting an unexpected role for LTβR signaling in central tolerance induction.