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Prepublished online as a Blood First Edition Paper on April 17, 2003; DOI 10.1182/blood-2003-01-0316.
Submitted January 31, 2003
Accepted April 5, 2003
Changes in the lymph node microenvironment induced by Oncostatin M
Isabelle Louis, Gael Dulude, Sophie Corneau, Sylvie Brochu, Catherine Boileau, Caroline Meunier, Caroline Cote, Nathalie Labrecque, and Claude Perreault*
Guy-Bernier Research Center, Maisonneuve-Rosemont Hospital, Montreal, PQ, Canada
* Corresponding author; email: c.perreault{at}videotron.ca.
Oncostatin M (OM) transforms the lymph node (LN) into a "super lymphoid organ" with two striking features: massive thymus-independent T cell development and major expansion of the memory T cell pool. We report that T cell development in the LckOM LN is regulated by a COX-2 dependent neoangiogenesis involving high endothelial venules (HEVs). That LN HEVs are particularly rich in OM-receptor  -chain provides a plausible explanation for the fact that extrathymic T cell development in LckOM mice is limited to the LN. Moreover, we found that increased production of the CCL20 chemokine by LN stromal cells was instrumental in the expansion of the memory phenotype CD4 T cell pool in LckOM mice. The generality of the latter finding was demonstrated by the fact that CCL20-CCR6 interactions increase the basal proliferation rate of CD62Llo CD4 T cells irrespective of their thymic (in non OM transgenic mice) or extrathymic (in LckOM mice) origin. To our knowledge, CCL20 is the first molecule found to increase the proliferation of memory phenotype CD4 T cells. These findings identify potential targets for the creation of thymic substitutes (LN HEVs) and for expansion of the CD4 memory T cell compartment (CCL20).
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