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A B cell–dependent mechanism restrains T cell transendothelial migration

Nature Medicine volume 21, pages 424–426 (2015)Cite this article

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A new study reveals that B cells restrict the transendothelial migration of T cells in physiological inflammation in response to adiponectin, but that this mechanism is compromised in autoimmunity and is hence a novel avenue for therapy development.

The authors made their discovery while investigating adiponectin's effect on lymphocyte migration1. Adiponectin is an adipokine involved in metabolism, adipogenesis and diabetes. Recently, adiponectin and its receptors AdipoR1 and AdipoR2 were shown to inhibit leukocyte recruitment to inflamed endothelium2. Furthermore, low levels of circulating adiponectin have been observed in some diseases, including diabetes3. To explore adiponectin's influence on lymphocyte TEM in detail, the authors carried out in vitro transmigration assays, isolating peripheral blood lymphocytes (PBLs) from healthy individuals and following their movement across confluent monolayers of TNF-α– and IFN-γ–stimulated endothelial cells by video-microscopy.

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Figure 1: The role of B cells in S1P-mediated regulation of T cell trafficking.

Kim Caesar/Nature Publishing Group

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  1. Julie D. Saba is at the Children's Hospital Oakland Research Institute, University of California, San Francisco (UCSF) Benioff Children's Hospital Oakland, Oakland, California, USA.,

    Julie D Saba

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  1. Julie D Saba
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Correspondence to Julie D Saba.

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Saba, J. A B cell–dependent mechanism restrains T cell transendothelial migration. Nat Med 21, 424–426 (2015). https://doi.org/10.1038/nm.3858

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