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Identification of a New Member of the CD20/FcεRIβ Family Overexpressed in Tolerated Allografts
Author(s) -
Louvet Cédric,
Chiffoleau Elise,
Heslan Michèle,
Tesson Laurent,
Heslan JeanMarie,
Brion Régis,
Bériou Gaëlle,
Guillonneau Carole,
Khalife Jamal,
Anegon Ignacio,
Cuturi MariaCristina
Publication year - 2005
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2005.01007.x
Subject(s) - cd86 , immune system , bone marrow , immunology , myeloid , immune tolerance , medicine , cd19 , major histocompatibility complex , monocyte , gene , heart transplantation , microbiology and biotechnology , biology , t cell , transplantation , genetics , surgery
We identified a novel rat gene specifically overexpressed in tolerated heart allografts in a model of tolerance induced by donor‐specific blood transfusion (DST). We named this gene TORID, for tolerance‐related and induced transcript. We show that TORID expression can be attributed to non‐T cells infiltrating tolerated grafts. Interestingly, TORID overexpression was also observed in long‐term grafts from a different model of tolerance in which chronic rejection does not occur. Comparison of the predicted amino acid sequence of TORID and of its human counterpart LR8 showed an homology with the four‐transmembrane CD20/FcεRIβ family proteins. We investigated TORID expression in naive rat immune cells and lymphoid tissues. TORID was found to be preferentially expressed in cells of the myeloid lineage such as macrophages and dendritic cells (DCs). Its expression dramatically decreased following activation/maturation. Similar results were obtained in human monocyte‐derived DCs. Interestingly, TORID overexpression in bone marrow‐derived DCs alters expression of MHC II and CD86 and production of IL12p40 following activation. These results suggest that TORID may be involved in the control of DC maturation and may, therefore, play a role in the induction or maintenance of allograft tolerance.