Dataset Information

Fluorescence tagging and inducible depletion of PD-L2-expressing B-1 B cells in vivo.

ABSTRACT: L2pB1 cells are a subpopulation of B-1a B cells that express programmed death ligand 2 (PD-L2) as their unique cell surface marker. In mice, about 50% of peritoneal B-1a cells are L2pB1 cells. The remaining B-1a cells are L2nB1 (PD-L2(-) ) B-1a cells. L2pB1 cells differ from L2nB1 cells in their immunoglobulin repertoire, expression of interleukin 10, and their capacity to phagocytose phosphatidylcholine. The physiological roles of L2pB1 cells have not been investigated owing to the lack of an animal model that allows for specific depletion of L2pB1 cells. Here, we report a mouse model that enables specific tracking and inducible depletion of L2pB1 cells in vivo. Our data show that depletion of L2pB1 cells significantly reduces serum anti-phosphorylcholine (PC) IgM levels and IL-10 expression in the peritoneal cavity. This animal model provides a tool for the study of the immune regulatory functions of L2pB1 cells in health and disease.

SUBMITTER: Lee RA

PROVIDER: S-EPMC4679664 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature

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Publications

Fluorescence tagging and inducible depletion of PD-L2-expressing B-1 B cells in vivo.

Lee Rebecca A RA Mao Changchuin C Vo Hung H Gao Wenda W Zhong Xuemei X

Annals of the New York Academy of Sciences 20150820

L2pB1 cells are a subpopulation of B-1a B cells that express programmed death ligand 2 (PD-L2) as their unique cell surface marker. In mice, about 50% of peritoneal B-1a cells are L2pB1 cells. The remaining B-1a cells are L2nB1 (PD-L2(-) ) B-1a cells. L2pB1 cells differ from L2nB1 cells in their immunoglobulin repertoire, expression of interleukin 10, and their capacity to phagocytose phosphatidylcholine. The physiological roles of L2pB1 cells have not been investigated owing to the lack of an a ...[more]

PMID: 26291441

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Project description:Classical Hodgkin lymphomas (cHLs) include small numbers of malignant Reed-Sternberg cells within an extensive but ineffective inflammatory/immune cell infiltrate. In cHL, chromosome 9p24.1/PD-L1/PD-L2 alterations increase the abundance of the PD-1 ligands, PD-L1 and PD-L2, and their further induction through Janus kinase 2-signal transducers and activators of transcription signaling. The unique composition of cHL limits its analysis with high-throughput genomic assays. Therefore, the precise incidence, nature, and prognostic significance of PD-L1/PD-L2 alterations in cHL remain undefined.We used a fluorescent in situ hybridization assay to evaluate CD274/PD-L1 and PDCD1LG2/PD-L2 alterations in 108 biopsy specimens from patients with newly diagnosed cHL who were treated with the Stanford V regimen and had long-term follow-up. In each case, the frequency and magnitude of 9p24.1 alterations-polysomy, copy gain, and amplification-were determined, and the expression of PD-L1 and PD-L2 was evaluated by immunohistochemistry. We also assessed the association of 9p24.1 alterations with clinical parameters, which included stage (early stage I/II favorable risk, early stage unfavorable risk, advanced stage [AS] III/IV) and progression-free survival (PFS).Ninety-seven percent of all evaluated cHLs had concordant alterations of the PD-L1 and PD-L2 loci (polysomy, 5% [five of 108]; copy gain, 56% [61 of 108]; amplification, 36% [39 of 108]). There was an association between PD-L1 protein expression and relative genetic alterations in this series. PFS was significantly shorter for patients with 9p24.1 amplification, and the incidence of 9p24.1 amplification was increased in patients with AS cHL.PD-L1/PD-L2 alterations are a defining feature of cHL. Amplification of 9p24.1 is more common in patients with AS disease and associated with shorter PFS in this series. Further analyses of 9p24.1 alterations in patients treated with standard cHL induction regimens or checkpoint blockade are warranted.

Dataset Information

Fluorescence tagging and inducible depletion of PD-L2-expressing B-1 B cells in vivo.

Publications

Fluorescence tagging and inducible depletion of PD-L2-expressing B-1 B cells in vivo.

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