First Author | Funakoshi S | Year | 2015 |
Journal | PLoS One | Volume | 10 |
Issue | 1 | Pages | e0117566 |
PubMed ID | 25612318 | Mgi Jnum | J:225656 |
Mgi Id | MGI:5693994 | Doi | 10.1371/journal.pone.0117566 |
Citation | Funakoshi S, et al. (2015) BILL-cadherin/cadherin-17 contributes to the survival of memory B cells. PLoS One 10(1):e0117566 |
abstractText | Memory B cells (MBCs) and long-lived plasma cells (LLPCs) are responsible for immunological "memory", which can last for many years. The long-term survival niche for LLPCs in the bone marrow is well characterized; however, the corresponding niche for MBCs is unclear. BILL-cadherin/cadherin-17 (CDH17) is the only member of the cadherin superfamily that is expressed on mouse B lymphocytes in a spatiotemporally regulated manner. Here, we show that half of all MBCs regain expression of CDH17 during the later stage of development. The maintenance of high affinity antigen-specific serum antibodies was impaired in CDH17(-/-) mice and the number of antigen-specific MBCs was reduced as compared to wild-type mice (WT). Also, specific responses to secondary antigens were ablated in CDH17(-/-) mice, whereas primary antibody responses were the same as those in WT mice. Cell cycle analysis revealed a decline in the proliferation of CDH17(-) MBCs as compared to CDH17(+) MBCs. In addition, we identified a subpopulation of splenic stromal cells, MAdCAM-1(+) blood endothelial cells (BEC), which was CDH17(+). Taken together, these results suggest that CDH17 plays a role in the long-term survival of MBCs, presumably via an "MBC niche" comprising, at least in part, BEC in the spleen. |