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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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Published on: September 26, 2013

Thymic medullary epithelial cell differentiation, thymocyte emigration, and the control of autoimmunity require

Thomas Boehm1, Stefanie Scheu, Klaus Pfeffer

  • 1Max Planck Institute for Immunobiology, Stuebeweg 51, 79108 Freiburg, Germany.

The Journal of Experimental Medicine
|September 4, 2003
PubMed

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 beta receptor (LTbetaR) signaling axis. Normal differentiation of thymic MECs requires LTbetaR ligand on thymocytes and LTbetaR together with nuclear factor-kappaB-inducing kinase (Nik) in thymic epithelial cells. Impaired lympho-epithelial cross talk in the absence of the LTbetaR 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 LTbetaR signaling in central tolerance induction.

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