Expression profiles of novel cell surface molecules on B-cell subsets and plasma cells as analyzed by flow cytometry

Llinàs, Laia; Lázaro, Adriana; Salort, José de; Matesanz-Isabel, Jessica; Sintes, Jordi; Engel, Pablo

doi:10.1016/j.imlet.2010.10.009

Cited by 39 publications

(28 citation statements)

References 19 publications

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“…CLCF1 encodes cardiotrophin-like-cytokine factor 1, which binds to CRLF1 to form a compound cytokine, eventually leading to activation of the JAK-STAT signaling and B-cell proliferation in vivo (Senaldi et al 2002;Crabe et al 2009;Savin et al 2015;Sims 2015). Important for lymphocyte development and activation, BTLA expression is highly regulated during B-cell differentiation and is also directly linked to B-cell receptor signaling cascade (Vendel et al 2009;Llinas et al 2011;Kannan et al 2015). Because ZNF384 binding sites were identified within the promoter and enhancer regions of both BTLA and CLCF1 (Supplemental Fig.…”

Section: Resultsmentioning

confidence: 99%

Whole-transcriptome sequencing identifies a distinct subtype of acute lymphoblastic leukemia with predominant genomic abnormalities of EP300 and CREBBP

et al. 2016

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Chromosomal translocations are a genomic hallmark of many hematologic malignancies. Often as initiating events, these structural abnormalities result in fusion proteins involving transcription factors important for hematopoietic differentiation and/or signaling molecules regulating cell proliferation and cell cycle. In contrast, epigenetic regulator genes are more frequently targeted by somatic sequence mutations, possibly as secondary events to further potentiate leukemogenesis. Through comprehensive whole-transcriptome sequencing of 231 children with acute lymphoblastic leukemia (ALL), we identified 58 putative functional and predominant fusion genes in 54.1% of patients (n = 125), 31 of which have not been reported previously. In particular, we described a distinct ALL subtype with a characteristic gene expression signature predominantly driven by chromosomal rearrangements of the ZNF384 gene with histone acetyltransferases EP300 and CREBBP. ZNF384-rearranged ALL showed significant up-regulation of CLCF1 and BTLA expression, and ZNF384 fusion proteins consistently showed higher activity to promote transcription of these target genes relative to wild-type ZNF384 in vitro. Ectopic expression of EP300-ZNF384 and CREBBP-ZNF384 fusion altered differentiation of mouse hematopoietic stem and progenitor cells and also potentiated oncogenic transformation in vitro. EP300-and CREBBP-ZNF384 fusions resulted in loss of histone lysine acetyltransferase activity in a dominant-negative fashion, with concomitant global reduction of histone acetylation and increased sensitivity of leukemia cells to histone deacetylase inhibitors. In conclusion, our results indicate that gene fusion is a common class of genomic abnormalities in childhood ALL and that recurrent translocations involving EP300 and CREBBP may cause epigenetic deregulation with potential for therapeutic targeting.

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Section: Resultsmentioning

confidence: 99%

Whole-transcriptome sequencing identifies a distinct subtype of acute lymphoblastic leukemia with predominant genomic abnormalities of EP300 and CREBBP

et al. 2016

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“…Trafficking across the epithelial layer of the choroid plexus appears to be critically driven by binding of CCL20, a chemokine constitutively expressed in human choroid plexus epithelial cells to its counter-receptor CCR6 on Th-17 T cells and other T-cell subsets, as demonstrated in a very elegant recent study [20]. Although it remains to be determined whether other chemokines are involved in immune cell diapedesis at the interface between blood and CSF, CCR6 is also expressed on several BC-subsets [21], as are leukocyte function-associated antigen 1 (LFA-1) and P-selectin glycoprotein ligand 1 (PSGL-1), the ligands of ICAM-1 and P-selectin [22]. Both LFA-1/ICAM-1 and very late antigen 4 (VLA-4)/fibronection interaction were required to mediate BC-migration in an in vitro BBB model [23].…”

Section: Discussionmentioning

confidence: 96%

B cells undergo unique compartmentalized redistribution in multiple sclerosis

Haas

Bekeredjian‐Ding

Milkova

et al. 2011

Journal of Autoimmunity

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“…Whereas pre/pro and most immature B cells do not express CCR6, loss of CD10 and maturation into the surface IgD + mature B cell pool leads to its acquisition (53). CCR6 is expressed by all naive follicular and pre-GC B cells in mice and humans but is absent from GC B cells and plasma cells (18,(53)(54)(55), suggesting a critical role for positioning to the mantle zone or corona around the developing GC in the follicle (56). Moreover, recent reports demonstrate a rapid and high acquisition of CCR6 on a precursor B cell population that can develop into switched or unswitched memory B cells in a GC-independent fashion (24,55,57).…”

Section: Discussionmentioning

confidence: 99%

A TNF-α–CCL20–CCR6 Axis Regulates Nod1-Induced B Cell Responses

Paradis

Mindt

Duerr

et al. 2014

The Journal of Immunology

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Innate immune responses provoke the accumulation of leukocytes at sites of inflammation. In addition to monocytes and granulocytes, B cells also participate in antimicrobial innate immune responses; however, the mechanisms for accumulation of B cells to sites of inflammation are not well understood. To study B cell accumulation following systemic inflammation, we used a model synthetic ligand that stimulates a specific pattern recognition molecule, nucleotide-binding oligomerization domain–containing protein 1 (Nod1). Upon exposure to Nod1 agonists, both B cells and neutrophils rapidly accumulate within the spleen, and dendritic cells migrate into the periarterial lymphoid sheath. Nod1 stimulation led to a marked increase in several chemokines within the spleen, including CXCL13, CCL2, and CCL20. Whereas the lymphotoxin pathway was critical for the induction of the B cell chemoattractant CXCL13 in response to Nod1 agonists, B cell accumulation within the spleen following Nod1-induced systemic inflammation was independent of the lymphotoxin pathway. In contrast, a CCR6/CCL20 chemokine loop instructed rapid increase of B cells in the spleen in response to systemic administration of Nod1 agonists in a TNF-α–dependent manner. Moreover, CCR6 was required to regulate Nod1-mediated B cell responses. These results reveal a novel mechanism of B cells during inflammation and shed light on how B cells participate in innate immune responses to microbial stimulation.

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Expression profiles of novel cell surface molecules on B-cell subsets and plasma cells as analyzed by flow cytometry

Cited by 39 publications

References 19 publications

Whole-transcriptome sequencing identifies a distinct subtype of acute lymphoblastic leukemia with predominant genomic abnormalities of EP300 and CREBBP

Whole-transcriptome sequencing identifies a distinct subtype of acute lymphoblastic leukemia with predominant genomic abnormalities of EP300 and CREBBP

B cells undergo unique compartmentalized redistribution in multiple sclerosis

A TNF-α–CCL20–CCR6 Axis Regulates Nod1-Induced B Cell Responses

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