EBI2 Expression and Function: Robust in Memory Lymphocytes and Increased by Natalizumab in Multiple Sclerosis

Publication date: 3 January 2017
Source:Cell Reports, Volume 18, Issue 1
Author(s): Aurélie S. Clottu, Amandine Mathias, Andreas W. Sailer, Myriam Schluep, Jörg D. Seebach, Renaud Du Pasquier, Caroline Pot
The interaction between oxysterols and the G protein-coupled receptor Epstein-Barr virus-induced gene 2 (EBI2) fine-tunes immune cell migration, a mechanism efficiently targeted by several disease-modifying treatments developed to treat multiple sclerosis (MS), such as natalizumab. We previously showed that memory CD4⁺ T lymphocytes migrate specifically in response to 7α,25-dihydroxycholesterol (7α,25-OHC) via EBI2 in the MS murine model experimental autoimmune encephalomyelitis. However, the EBI2 expression profile in human lymphocytes in both healthy and MS donors is unknown. Here, we characterize EBI2 biology in human lymphocytes. We observed that EBI2 is functionally expressed on memory CD4⁺ T cells and is enhanced under natalizumab treatment. These data suggest a significant role for EBI2 in human CD4⁺ T cell migration, notably in patients with MS. Better knowledge of EBI2 involvement in autoimmunity may therefore lead to an improved understanding of the physiopathology of MS.

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Teaser

Clottu et al. investigated the expression and function of the oxysterol receptor EBI2 in human primary lymphocytes. They show that EBI2 regulates human lymphocyte migration in vitro and that its expression and migratory response are increased in memory CD4⁺ T cells from multiple sclerosis patients treated with natalizumab.


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