期刊
BLOOD
卷 117, 期 20, 页码 5413-5424出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2010-11-317115
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资金
- Arthritis Research UK
- Biotechnology and Biological Sciences Research Council
- Medical Research Council
- Wellcome Trust
- Biotechnology and Biological Sciences Research Council [BB/G010773/1] Funding Source: researchfish
- Medical Research Council [G0901113, G0600856] Funding Source: researchfish
- BBSRC [BB/G010773/1] Funding Source: UKRI
- MRC [G0901113, G0600856] Funding Source: UKRI
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 Ca2+ 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 classswitched 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. (Blood. 2011;117(20):5413-5424)
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