Immunophenotypic analysis and quantification of B-1 and B-2 B cells during human fetal hematopoietic development

Bueno, Clara; Roon, Eddy H.J. Van; Muñoz‐López, Álvaro; Sanjuán-Pla, Alejandra; Juan, Manel; Navarro, Alfons; Stam, Ronald W.; Menéndez, Pablo

doi:10.1038/leu.2015.362

Cited by 17 publications

(16 citation statements)

References 19 publications

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“…Although human CD5+CD43+ B cells have not been clearly characterized and whether these cells are equivalent to B-1a cells in mice is unclear, some studies support the hypothesis that a subset of B cells possessing the characteristics of B-1a cells of mice exists in humans. [48][49][50][51] These B-1a-like cells may be the origin of the CD5+CD43+ cells in DLBCL, which warrants further investigation. CD5 and CD43 may be involved in the pathogenesis of DLBCL through a variety of mechanisms.…”

Section: Discussionmentioning

confidence: 93%

Coexpression of CD5 and CD43 predicts worse prognosis in diffuse large B‐cell lymphoma

Zhong

Zheng

et al. 2018

Cancer Medicine

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Both CD5 and CD43 are expressed on the surface of B lymphocytes of definite phase and associated with the adverse outcome in diffuse large B‐cell lymphoma (DLBCL). However, the relationship between CD5 and CD43 expression and the prognostic value of CD5/CD43 coexpression in DLBCL are unknown. We herein determined the correlation between CD5 and CD43 expression, as separate factors or in combination, with the clinicopathological features and survival of 200 patients with DLBCL receiving standard chemotherapy with or without rituximab. Among these DLBCL patients, CD5 expression, CD43 expression, and CD5/CD43 coexpression were detected in 18 (9%), 57 (27%), and 10 (5%) patients, respectively, and all were positively correlated with advanced age and nongerminal cell type. CD5‐positive and CD43‐positive DLBCL patients had poorer event‐free survival (EFS, P < 0.001) and overall survival (OS, P < 0.001) than CD5‐negative and CD43‐negative patients, respectively. CD5/CD43 coexpression was correlated with a significantly worse prognosis than CD5 or CD43 expression alone. Univariate analysis showed that CD5 expression, CD43 expression, and CD5/CD43 coexpression were all adverse prognostic factors for DLBCL patient survival, and CD5/CD43 coexpression was associated with a greater relative risk for recurrence and death than either CD5 or CD43 expression alone. Multivariate analysis demonstrated that CD5/CD43 coexpression was an independent prognostic factor for EFS (P < 0.001) and OS (P < 0.001) in DLBCL. In conclusion, our data indicate that DLBCL patients with CD5/CD43 coexpression represent a specific subgroup with a significantly worse prognosis than those expressing either marker alone.

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Section: Discussionmentioning

confidence: 93%

Coexpression of CD5 and CD43 predicts worse prognosis in diffuse large B‐cell lymphoma

Zhong

Zheng

et al. 2018

Cancer Medicine

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“…However, and in line with previous work ( Munoz-Lopez et al., 2016 ), Epstein-Barr virus (EBV)-immortalized healthy B cells as well as healthy pro-B and pre-B cells could be successfully reprogrammed ( Figure S2 C), suggesting that the leukemia-initiating event (e.g., MLL fusion genes) may represent a reprogramming barrier. To test this idea, we lentivirally transduced both CB-CD34 + hematopoietic stem/progenitor cells (HSPCs) and CD34 + CD19 + B cell progenitors with MLL-AF4-GFP, and after several days infected MLL-AF4-expressing CD34 + and CD34 + CD19 + cells with OKSM-SeV ( Bueno et al., 2015 ). MLL-AF4 expression did not impair the generation of iPSCs, and the reprogramming efficiency was similar to that of GFP-transduced CD34 + HSPCs ( Figure 3 A) and CD34 + CD19 + B cell progenitors ( Figure S3 A).…”

Section: Resultsmentioning

confidence: 99%

“…A one- or two-round sorting strategy was used as indicated with resulting purities >99% and practically 100%, respectively ( Figure 1 A and Table 1 ). CB-derived CD34 + HSPCs and FL-derived CD34 + CD19 + B cell HPCs were processed as described previously ( Bueno et al., 2015 , Munoz-Lopez et al., 2016 , Prieto et al., 2016 , Ramos-Mejia et al., 2012d ). Where indicated, CD34 + cells were lentivirally transduced with MLL-AF4-GFP as reported ( Montes et al., 2014 ) and MLL-AF4-GFP-expressing CD34 + cells were FACS enriched for iPSC generation and DNA methylome studies (see below).…”

Section: Methodsmentioning

confidence: 99%

Development Refractoriness of MLL-Rearranged Human B Cell Acute Leukemias to Reprogramming into Pluripotency

et al. 2016

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SummaryInduced pluripotent stem cells (iPSCs) are a powerful tool for disease modeling. They are routinely generated from healthy donors and patients from multiple cell types at different developmental stages. However, reprogramming leukemias is an extremely inefficient process. Few studies generated iPSCs from primary chronic myeloid leukemias, but iPSC generation from acute myeloid or lymphoid leukemias (ALL) has not been achieved. We attempted to generate iPSCs from different subtypes of B-ALL to address the developmental impact of leukemic fusion genes. OKSM(L)-expressing mono/polycistronic-, retroviral/lentiviral/episomal-, and Sendai virus vector-based reprogramming strategies failed to render iPSCs in vitro and in vivo. Addition of transcriptomic-epigenetic reprogramming “boosters” also failed to generate iPSCs from B cell blasts and B-ALL lines, and when iPSCs emerged they lacked leukemic fusion genes, demonstrating non-leukemic myeloid origin. Conversely, MLL-AF4-overexpressing hematopoietic stem cells/B progenitors were successfully reprogrammed, indicating that B cell origin and leukemic fusion gene were not reprogramming barriers. Global transcriptome/DNA methylome profiling suggested a developmental/differentiation refractoriness of MLL-rearranged B-ALL to reprogramming into pluripotency.

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“…Subsequent waves of HSC-derived B-1 and adaptive B-2 lymphocytes arise later in the foetal liver (Yoshimoto, 2015) and a wave of predominantly HSC-derived B-2 lymphocytes emerges in the bone marrow (Montecino-Rodriguez and Dorshkind, 2012). The identification of B-1 lymphocytes in humans (Rothstein and Quach, 2015), and their observation in the 10-11 week foetal liver (Bueno et al, 2016), argues for conservation of the innate immune system between species. Given that human B-1 cells differ immunophenotypically from B-2 lymphocytes (Rothstein and Quach, 2015), it should therefore be possible to discern whether B cells derived from human hPSCs include B-2 cells, and are thus unequivocally descended from HSCs.…”

Section: Agm-like He D9-18mentioning

confidence: 99%

Human haematopoietic stem cell development: from the embryo to the dish

et al. 2017

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Haematopoietic stem cells (HSCs) emerge during embryogenesis and give rise to the adult haematopoietic system. Understanding how early haematopoietic development occurs is of fundamental importance for basic biology and medical sciences, but our knowledge is still limited compared with what we know of adult HSCs and their microenvironment. This is particularly true for human haematopoiesis, and is reflected in our current inability to recapitulate the development of HSCs from pluripotent stem cells in vitro. In this Review, we discuss what is known of human haematopoietic development: the anatomical sites at which it occurs, the different temporal waves of haematopoiesis, the emergence of the first HSCs and the signalling landscape of the haematopoietic niche. We also discuss the extent to which in vitro differentiation of human pluripotent stem cells recapitulates bona fide human developmental haematopoiesis, and outline some future directions in the field.

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Immunophenotypic analysis and quantification of B-1 and B-2 B cells during human fetal hematopoietic development

Cited by 17 publications

References 19 publications

Coexpression of CD5 and CD43 predicts worse prognosis in diffuse large B‐cell lymphoma

Coexpression of CD5 and CD43 predicts worse prognosis in diffuse large B‐cell lymphoma

Development Refractoriness of MLL-Rearranged Human B Cell Acute Leukemias to Reprogramming into Pluripotency

Human haematopoietic stem cell development: from the embryo to the dish

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