Cosmc controls B cell homing

Junwei Zeng, Mahmoud Eljalby, Rajindra P. Aryal, Sylvain Lehoux, Kathrin Stavenhagen, Matthew R. Kudelka, Yingchun Wang, Jianmei Wang, Tongzhong Ju, Ulrich H. Andrian and Richard D. Cummings ()
Additional contact information
Junwei Zeng: Harvard Medical School
Mahmoud Eljalby: Harvard Medical School
Rajindra P. Aryal: Harvard Medical School
Sylvain Lehoux: Harvard Medical School
Kathrin Stavenhagen: Harvard Medical School
Matthew R. Kudelka: Harvard Medical School
Yingchun Wang: Emory University
Jianmei Wang: Emory University
Tongzhong Ju: Emory University
Ulrich H. Andrian: Harvard Medical School
Richard D. Cummings: Harvard Medical School

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract The molecular mechanisms regulating lymphocyte homing into lymph nodes are only partly understood. Here, we report that B cell-specific deletion of the X-linked gene, Cosmc, and the consequent decrease of protein O-glycosylation, induces developmental blocks of mouse B cells. After transfer into wild-type recipient, Cosmc-null B cells fail to home to lymph nodes as well as non-lymphoid organs. Enzymatic desialylation of wild-type B cells blocks their migration into lymph nodes, indicating a requirement of sialylated O-glycans for proper trafficking. Mechanistically, Cosmc-deficient B cells have normal rolling and firm arrest on high endothelium venules (HEV), thereby attributing their inefficient trafficking to alterations in the subsequent transendothelial migration step. Finally, Cosmc-null B cells have defective chemokine signaling responses. Our results thus demonstrate that Cosmc and its effects on O-glycosylation are important for controlling B cell homing.

Date: 2020
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DOI: 10.1038/s41467-020-17765-6

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