Abstract
The present chapter aims at over-viewing molecular biological and functional characters of Prolymphocytes cells, describing cell-specific alterations of cellular functions, phenotypes and mediator productions in pathological conditions, exploring new understanding of cellular mechanisms on basis of findings from genomics, proteomics studies, defining disease-specific biomarkers and targets in these cells and the potential of target-associated therapies as well.
Prolymphocytes are the immediate precursor of a lymphocyte, derived from a lymphoblast, a developmental form in the lymphocytic series, intermediate between the lymphoblast and lymphocyte.
Pro-B-lymphocytes (pro-B-cells), that develop from hematopoietic progenitor cells, are an early identifiable intermediate cell type in a series of developmental stages leading to the generation of mature B-cells.
Similar to B cell maturation, T cell maturation also involves rearrangements of T cell receptor (TCR) genes and the expression of various membrane markers. Common lymphoid progenitors (CLPs) migrate from the embryonic liver or from adult bone marrow to colonize the thymus, the site of education and maturation of T lymphocyte. Several cytokines, that act together to promote early T-cell development, are also involved in prethymic development, such as the generation of CLPs and the maintenance of hematopoietic stem cells.
Aurora-A kinase is a cell-cycle-regulating kinase responsible for chromosomal segregation. Overexpression of Aurora-A kinase is correlate with tumor proliferation and chromosomal instability, thus Aurora-A kinase overexpression in chronic lymphocytic leukemia (CLL) may be involved in the genesis of chromosomal abnormalities and also is a potential target for therapeutic intervention.
Evidence from recent research indicate the possible relationship between the presence of malignant lymphocytes and their compact nucleoli in patient affected by chronic lymphocytic leukemia. Nucleolar test can be a possible prognostic parameter which can help identify the subset of patients that will run a more progressive course.
B-cell lymphocyte kinase (Blk), B-cell linker protein (BLNK), spleen tyrosine kinase (SYK), zeta-associated protein-70 (ZAP70) and iron-responsive element-binding protein 2 (IREB2) can be identified as important prolymphocyte related proteins that establish systemic interaction.
Cell development is also characterized by specific genes. Thirteen genes included in the Pubmed gene bank are related with prolymphocyte, while others genes play an important role during the maturation of T cells.
CLL is characterized by a level of Prolymphocytes >10 %. Current studies aim to find efficient biomarkers to characterize prognostic and phenotypic features of patients with CLL or prolymphocytic leukemia (PLL).
Although pro-B and pro-T cells have unique characters, both have specific characterization of lymphoid malignancy, and a better understanding of pro-B and pro-T is required. Thus, further studies must be conducted to provide an effective treatment of lymphoid malignancy.
Prolymphocytes are the immediate precursor of a lymphocyte, derived from a lymphoblast, a developmental form in the lymphocytic series, intermediate between the lymphoblast and lymphocyte.
Pro-B-lymphocytes (pro-B-cells), that develop from hematopoietic progenitor cells, are an early identifiable intermediate cell type in a series of developmental stages leading to the generation of mature B-cells.
Similar to B cell maturation, T cell maturation also involves rearrangements of T cell receptor (TCR) genes and the expression of various membrane markers. Common lymphoid progenitors (CLPs) migrate from the embryonic liver or from adult bone marrow to colonize the thymus, the site of education and maturation of T lymphocyte. Several cytokines, that act together to promote early T-cell development, are also involved in prethymic development, such as the generation of CLPs and the maintenance of hematopoietic stem cells.
Aurora-A kinase is a cell-cycle-regulating kinase responsible for chromosomal segregation. Overexpression of Aurora-A kinase is correlate with tumor proliferation and chromosomal instability, thus Aurora-A kinase overexpression in chronic lymphocytic leukemia (CLL) may be involved in the genesis of chromosomal abnormalities and also is a potential target for therapeutic intervention.
Evidence from recent research indicate the possible relationship between the presence of malignant lymphocytes and their compact nucleoli in patient affected by chronic lymphocytic leukemia. Nucleolar test can be a possible prognostic parameter which can help identify the subset of patients that will run a more progressive course.
B-cell lymphocyte kinase (Blk), B-cell linker protein (BLNK), spleen tyrosine kinase (SYK), zeta-associated protein-70 (ZAP70) and iron-responsive element-binding protein 2 (IREB2) can be identified as important prolymphocyte related proteins that establish systemic interaction.
Cell development is also characterized by specific genes. Thirteen genes included in the Pubmed gene bank are related with prolymphocyte, while others genes play an important role during the maturation of T cells.
CLL is characterized by a level of Prolymphocytes >10 %. Current studies aim to find efficient biomarkers to characterize prognostic and phenotypic features of patients with CLL or prolymphocytic leukemia (PLL).
Although pro-B and pro-T cells have unique characters, both have specific characterization of lymphoid malignancy, and a better understanding of pro-B and pro-T is required. Thus, further studies must be conducted to provide an effective treatment of lymphoid malignancy.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Aoki K, et al. A thymus-specific noncoding RNA, Thy-ncR1, is a cytoplasmic riboregulator of MFAP4 mRNA in immature T-cell lines. BMC Mol Biol. 2010;11:99.
Azulay-Debby H, Edry E, Melamed D. CpG DNA stimulates autoreactive immature B cells in the bone marrow. Eur J Immunol. 2007;37(6):1463–75.
Barr PM, et al. Syk inhibition with fostamatinib leads to transitional B lymphocyte depletion. Clin Immunol. 2012;142(3):237–42.
Bell JJ, Bhandoola A. The earliest thymic progenitors for T cells possess myeloid lineage potential. Nature. 2008;452(7188):764–7.
Boxer LM, Dang CV. Translocations involving c-myc and c-myc function. Oncogene. 2001;20(40):5595–610.
Bustany S, Tchakarska G, Sola B. Cyclin D1 regulates p27(Kip1) stability in B cells. Cell Signal. 2011;23(1):171–9.
Chen L, et al. Expression of ZAP-70 is associated with increased B-cell receptor signaling in chronic lymphocytic leukemia. Blood. 2002;100(13):4609–14.
Cheng S, et al. BCR-mediated apoptosis associated with negative selection of immature B cells is selectively dependent on Pten. Cell Res. 2009;19(2):196–207.
Degner SC, et al. CCCTC-binding factor (CTCF) and cohesin influence the genomic architecture of the Igh locus and antisense transcription in pro-B cells. Proc Natl Acad Sci U S A. 2011;108(23):9566–71.
Edry E, Azulay-Debby H, Melamed D. TOLL-like receptor ligands stimulate aberrant class switch recombination in early B cell precursors. Int Immunol. 2008;20(12):1575–85.
Hoehn D, et al. Splenic B-cell lymphomas with more than 55% prolymphocytes in blood: evidence for prolymphocytoid transformation. Hum Pathol. 2012;43(11):1828–38.
Huh YO, et al. MYC translocation in chronic lymphocytic leukaemia is associated with increased prolymphocytes and a poor prognosis. Br J Haematol. 2008;142(1):36–44.
Inamdar KV, et al. Aurora-A kinase nuclear expression in chronic lymphocytic leukemia. Mod Pathol. 2008;21(12):1428–35.
Klein WR, et al. The intrathymic crossroads of T and NK cell differentiation. Immunol Rev. 2010;238(1):126–37.
Klobusicka M, et al. Possible prognostic value of nucleolar morphology in pathologic cells of B-chronic lymphocytic leukemia. Neoplasma. 2010;57(5):429–37.
Kondo M. Lymphoid and myeloid lineage commitment in multipotent hematopoietic progenitors. Immunol Rev. 2010;238(1):37–46.
Laslo P, et al. Gene regulatory networks directing myeloid and lymphoid cell fates within the immune system. Semin Immunol. 2008;20(4):228–35.
Lens D, et al. p53 abnormalities in CLL are associated with excess of prolymphocytes and poor prognosis. Br J Haematol. 1997;99(4):848–57.
Lu TP, et al. Distinct signaling pathways after higher or lower doses of radiation in three closely related human lymphoblast cell lines. Int J Radiat Oncol Biol Phys. 2010;76(1):212–19.
Martensson IL, et al. The pre-B cell receptor checkpoint. FEBS Lett. 2010;584(12):2572–9.
Minegishi Y, et al. An essential role for BLNK in human B cell development. Science. 1999;286(5446):1954–7.
Nakashima H, et al. Splenic irradiation as a successful treatment for an elderly patient with B-cell prolymphocytic leukemia. Rinsho Ketsueki. 2008;49(12):1619–22.
Nakayama J, et al. BLNK suppresses pre-B-cell leukemogenesis through inhibition of JAK3. Blood. 2009;113(7):1483–92.
Niiro H, Clark EA. Regulation of B-cell fate by antigen-receptor signals. Nat Rev Immunol. 2002;2(12):945–56.
Nimer SD. MDS: a stem cell disorder – but what exactly is wrong with the primitive hematopoietic cells in this disease? Hematol Am Soc Hematol Educ Program. 2008;2008:43–51.
Northrup DL, Allman D. Transcriptional regulation of early B cell development. Immunol Res. 2008;42(1–3):106–17.
Ozaki S, et al. A case of T-cell prolymphocytic leukemia. Rinsho Ketsueki. 1992;33(6):817–22.
Phillips JE, Corces VG. CTCF: master weaver of the genome. Cell. 2009;137(7):1194–211.
Put N, et al. Chronic lymphocytic leukemia and prolymphocytic leukemia with MYC translocations: a subgroup with an aggressive disease course. Ann Hematol. 2012;91(6):863–73.
Schultze FC, et al. Differential proteome and phosphoproteome signatures in human T-lymphoblast cells induced by sirolimus. Cell Prolif. 2010;43(4):396–404.
Smith EM, et al. Inhibition of EBF function by active Notch signaling reveals a novel regulatory pathway in early B-cell development. Blood. 2005;106(6):1995–2001.
Taghon T, et al. Homeobox gene expression profile in human hematopoietic multipotent stem cells and T-cell progenitors: implications for human T-cell development. Leukemia. 2003;17(6):1157–63.
Thoren LA, et al. Kit regulates maintenance of quiescent hematopoietic stem cells. J Immunol. 2008;180(4):2045–53.
Tokoyoda K, et al. Cellular niches controlling B lymphocyte behavior within bone marrow during development. Immunity. 2004;20(6):707–18.
Ueda Y, et al. Inflammation controls B lymphopoiesis by regulating chemokine CXCL12 expression. J Exp Med. 2004;199(1):47–58.
van der Meer LT, Jansen JH, van der Reijden BA. Gfi1 and Gfi1b: key regulators of hematopoiesis. Leukemia. 2010;24(11):1834–43.
Yang Q, Jeremiah BJ, Bhandoola A. T-cell lineage determination. Immunol Rev. 2010;238(1):12–22.
Yin CC, et al. Chronic lymphocytic leukemia With t(2;14)(p16;q32) involves the BCL11A and IgH genes and is associated with atypical morphologic features and unmutated IgVH genes. Am J Clin Pathol. 2009;131(5):663–70.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2015 Springer Science+Business Media Dordrecht
About this chapter
Cite this chapter
Qian, M., Spada, C., Wang, X. (2015). Prolymphocyte: Lymphocytes and Bioinformatics. In: Wang, X. (eds) Single Cell Sequencing and Systems Immunology. Translational Bioinformatics, vol 5. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-9753-5_8
Download citation
DOI: https://doi.org/10.1007/978-94-017-9753-5_8
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-017-9752-8
Online ISBN: 978-94-017-9753-5
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)