| First Author | Hansell CA | Year | 2011 |
| Journal | Blood | Volume | 117 |
| Issue | 20 | Pages | 5413-24 |
| PubMed ID | 21450903 | Mgi Jnum | J:173257 |
| Mgi Id | MGI:5013683 | Doi | 10.1182/blood-2010-11-317115 |
| Citation | Hansell CA, et al. (2011) Universal expression and dual function of the atypical chemokine receptor D6 on innate-like B cells in mice. Blood 117(20):5413-24 |
| abstractText | Mouse innate-like B cells are a heterogeneous collection of multifunctional cells that control infection, play housekeeping roles, contribute to adaptive immunity, and suppress inflammation. We show that, among leukocytes, chemokine internalization by the D6 receptor is a unique and universal feature of all known innate-like B-cell populations and, to our knowledge, the most effective unifying marker of these cells. Moreover, we identify novel D6(active) B1-cell subsets, including those we term B1d, which lack CD5 and CD11b but exhibit typical B1-cell properties, including spontaneous ex vivo production of IgM, IL-10, and anti-phosphorylcholine antibody. The unprecedented opportunity to examine D6 on primary cells has allowed us to clarify its ligand specificity and show that, consistent with a scavenging role, D6 internalizes chemokines but cannot induce Ca(2+) fluxes or chemotaxis. Unexpectedly, however, D6 can also suppress the function of CXCR5, a critical chemokine receptor in innate-like B-cell biology. This is associated with a reduction in B1 cells and circulating class-switched anti-phosphorylcholine antibody in D6-deficient mice. Therefore, in the present study, we identify a unifying marker of innate-like B cells, describe novel B1-cell subsets, reveal a dual role for D6, and provide the first evidence of defects in resting D6-deficient mice. |
