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PubMed1984

An immunofluorescence analysis of the ontogeny of myeloid, T, and B lineage cells in mouse hemopoietic tissues.

The population dynamics of granulopoietic cells, B-lineage cells, and T lymphocytes were analyzed by immunofluorescence in mouse hemopoietic tissues as a function of age. Mac-1+ myeloid cells were present on day 11 of gestation in the liver, where they peaked shortly after birth and declined subsequently. Waves of myeloid population growth began in spleen and bone marrow by days 15 and 19, respectively. Mac-1+ cells increased in number to relatively low plateau levels in spleen by the 3rd wk after birth, whereas in the bone marrow higher plateau levels were reached around 3 mo of age. The 14.8 monoclonal antibody was utilized as one marker of B-lineage precursor cells. 14.8+ cells were detected in the liver on day 11 of gestation, reached peak numbers during the first week after birth and decreased thereafter. On day 15 and 19, 14.8+ cells were found in spleen and bone marrow, respectively, and progressively increased in numbers to reach plateau levels in both sites by 3 mo of age. Mu+ pre-B cells appeared in significant numbers in the 13-day fetal liver, reached a peak shortly after birth, and disappeared from the liver by the end of the second postnatal week. Pre-B cells were found in the spleen and bone marrow on days 15 and 19, respectively. In the spleen pre-B cells reached peak values at birth and disappeared 2 wk later. In spite of the sequential appearance of mu+ pre-B cells in fetal liver, spleen, and bone marrow, their sIgM+ B cell progeny appeared in all these hemopoietic tissues on day 17 of gestation. In the liver, sIgM+ B cells reached their peak at birth and declined thereafter. In the spleen and bone marrow, B cells increased to plateau levels between 1 and 4 mo of age. Thy-1.2+ T cells were relatively late acquisitions in all three hemopoietic tissues. Finally, the expression of the 14.8 antigen by mu+ cells was examined as a function of gestational age. While pre-B cells from day-13 fetuses had no detectable 14.8 antigen, the antigen was weakly expressed on the vast majority of the mu+ pre-B cells by day 17 of gestation. Newborn liver cells expressing 14.8 antigen were found to include a small proportion of cells with peroxidase+ granules. Thus, demonstration of rearrangement and expression of immunoglobulin genes may be required for precise identification of cells of B lineage early in ontogeny.

Animals↗
PubMed2004

Bone marrow cells differentiate in cardiac cell lineages after infarction independently of cell fusion.

Recent studies in mice have challenged the ability of bone marrow cells (BMCs) to differentiate into myocytes and coronary vessels. The claim has also been made that BMCs acquire a cell phenotype different from the blood lineages only by fusing with resident cells. Technical problems exist in the induction of myocardial infarction and the successful injection of BMCs in the mouse heart. Similarly, the accurate analysis of the cell populations implicated in the regeneration of the dead tissue is complex and these factors together may account for the negative findings. In this study, we have implemented a simple protocol that can easily be reproduced and have reevaluated whether injection of BMCs restores the infarcted myocardium in mice and whether cell fusion is involved in tissue reconstitution. For this purpose, c-kit-positive BMCs were obtained from male transgenic mice expressing enhanced green fluorescence protein (EGFP). EGFP and the Y-chromosome were used as markers of the progeny of the transplanted cells in the recipient heart. By this approach, we have demonstrated that BMCs, when properly administrated in the infarcted heart, efficiently differentiate into myocytes and coronary vessels with no detectable differentiation into hemopoietic lineages. However, BMCs have no apparent paracrine effect on the growth behavior of the surviving myocardium. Within the infarct, in 10 days, nearly 4.5 million biochemically and morphologically differentiated myocytes together with coronary arterioles and capillary structures were generated independently of cell fusion. In conclusion, BMCs adopt the cardiac cell lineages and have an important therapeutic impact on ischemic heart failure.

Animals↗
PubMed1989

In vitro experiments on neuronal and glial cell lineages among the ventricular cells of the mouse neural plate.

The proliferative ventricular cells of the early neural plate of the mouse are generally assumed to be pluripotent and equivalent to one another in their developmental capability. Ventricular cells from the rostral parts of the neural plates of mice (Theiler stages 11 and 12, embryonic days 71/2 and 8) were studied in tissue culture with respect to their potential to give rise to neurons or glial cells, or both. Autoradiographic and immunohistochemical analyses showed that ventricular cells developing into neuronal phenotypes stopped proliferating immediately upon transfer to cell culture. Using polyclonal anti-GFAP antibodies, a small proportion of immunoreactive cells could be detected after 4 days of culture. These cells retained their proliferative activity, displayed morphological characteristics of radial glial cells, and may have either developed from specific glial progenitor cells or have been induced to proceed along the glial differentiation pathway at the beginning of culture. Therefore, two distinct types of progenitor cells, committed either to neuronal or glial lineages, appear to co-exist among the cultured neural plate ventricular cells.

Animals↗
PubMed2005

Transgenic expression of Helios in B lineage cells alters B cell properties and promotes lymphomagenesis.

Helios, a member of the Ikaros family of DNA-binding proteins, is expressed in multipotential lymphoid progenitors and throughout the T lineage. However, in most B lineage cells, Helios is not expressed, suggesting that its absence may be critical for B cell development and function. To test this possibility, transgenic mice were generated that express Helios under the control of an Ig mu enhancer. Commitment to the B cell lineage was unaltered in Helios transgenic mice, and numbers of surface IgM(+) B cells were normal in the bone marrow and spleen. However, both bone marrow and splenic B cells exhibited prolonged survival and enhanced proliferation. B cells in Helios transgenic mice were also hyperresponsive to Ag stimulation. These alterations were observed even though the concentration of ectopic Helios in B lineage cells, like that of endogenous Helios in thymocytes, was well below the concentration of Ikaros. Further evidence that ectopic Helios expression contributes to B cell abnormalities was provided by the observation that Helios transgenic mice developed metastatic lymphoma as they aged. Taken together, these results demonstrate that silencing of Helios is critical for normal B cell function.

Animals↗
PubMed1982

The cell-lineage of T gamma cells.

In patients with severe combined immunodeficiency, who have been successfully treated by bone-marrow transplantation, the occurrence of split take has been well documented: whereas myelomonocytic hemopoietic cell lines remain of host origin, the T-lymphoid compartment is of donor origin, while the B-lymphoid compartment may be either of host or of donor origin. We have studied the T gamma cells of two patients, successfully treated by bone-marrow transplantation from donors of the opposite sex, with respect to the sex-chromosome pattern, the binding of OKM1 and OKT3 monoclonal antibody and their K and NK activity. All T gamma cells of both patients were found to be of donor origin. These T gamma cells contained two serologically distinct subpopulations, one OKM1+ OKT3+, the other OKM1+ OKT3-, as was also found in normals. However, the ratio between these two subpopulations is 0.6 in normals, whereas these patients revealed a ratio of 3.0. Furthermore, the patients' T gamma cells displayed a strongly reduced K and NK activity (+/- 30% of normal). We concluded that at least part of the OKM1+ OKT3+ and of the OKM1+ OKT3- T gamma cells are derived from other than the myelomonocytic lineage, presumably from the lymphocytic lineage. The origin of the K and NK active T gamma cells, however, cannot be conclusively determined from these experiments. These findings also imply that the antigen detected by OKM1 should obviously no longer be regarded as exclusively present on myelomonocytic cells.

Antibodies, Monoclonal↗
PubMed1998

Human parvovirus B19 nonstructural (NS1) protein induces apoptosis in erythroid lineage cells.

Infection of erythroid-lineage cells by human parvovirus B19 is characterized by a gradual cytocidal effect. Accumulating evidence now implicates the nonstructural (NS1) protein of the virus in cytotoxicity, but the mechanism underlying the NS1-induced cell death is not known. Using a stringent regulatory system, we demonstrate that NS1 cytotoxicity is closely related to apoptosis, as evidenced by cell morphology, genomic DNA fragmentation, and cell cycle analysis with the human erythroleukemia cell line K562 and the erythropoietin-dependent megakaryocytic cell line UT-7/Epo. Apoptosis was significantly inhibited by an interleukin-1beta (IL-1beta)-converting enzyme (ICE)/CED-3 family protease inhibitor, Ac-DEVD-CHO (CPP32; caspase 3), whereas a similar inhibitor of ICE (caspase 1), Ac-YVAD-CHO, had no effect. Furthermore, stable expression of the human Bcl-2 proto-oncogene resulted in near-total protection from cell death in response to NS1 induction. Mutations engineered into the nucleoside triphosphate-binding domain of NS1 significantly rescued cells from NS1-induced apoptosis without having any effect on NS1-induced activation of the IL-6 gene expression which is mediated by NF-kappaB. Furthermore, using pentoxifylline, an inhibitor of NF-kappaB activation, we demonstrate that the NF-kappaB-mediated IL-6 activation by NS1 is uncoupled from the apoptotic pathway. This functional dissection indicates a complexity underlying the biochemical function of human parvovirus NS1 in transcriptional activation and induction of apoptosis. Our findings indicate that NS1 of parvovirus B19 induces cell death by apoptosis in at least erythroid-lineage cells by a pathway that involves caspase 3, whose activation may be a key event during NS1-induced cell death.

Apoptosis↗
PubMed1996

B-cell non-Hodgkin's lymphoma: evidence for the t (14;18) translocation in all hematopoietic cell lineages.

BACKGROUND: B cells of patients with non-Hodgkin's lymphoma (B-NHL) harbor specific chromosomal translocations, including t(14;18), the most common aberration found in this disease. The translocation involves the immunoglobulin (Ig) heavy-chain joining (JH) region gene on chromosome 14 and the BCL2 gene on chromosome 18, resulting in dysregulated expression of the BCL2 gene. The t(14;18) translocation has been thought to occur in the pre-B-cell stage, during the first event of Ig gene rearrangement. PURPOSE: This study was conducted to investigate the potential involvement of nonlymphoid lineages in B-NHL. METHODS: We studied the t(14;18) translocation and other frequently occurring translocations in total bone marrow aspirates of 10 patients with B-NHL, with the use of the fluorescence in situ hybridization (FISH) technique. We also performed cytogenetic analyses on representative bone marrow aspirates from the patients. Moreover, to define which of the major cell lineages present in the bone marrow carry the t(14;18) translocation, we used a series of monoclonal antibodies together with fluorescence-activated cell sorter (FACS) analyses to purify cells positive for CD3 (T cells), CD19 (B cells), CD10 (CALLA-positive cells), CD41a (megakaryocytic cells), CD13 (myeloid cells), and glycophorin A (erythroid cells). The cells of each subgroup underwent FISH analysis with the use of JH and BCL2 probes to detect the t(14;18) translocation. Bone marrow samples obtained from five healthy donors served as controls. RESULTS: Bone marrow cells from eight of the 10 patients studied carried the t(14;18) translocation. When present, the translocation was observed in many or even all of the cell lineages (lymphoid, myeloid, megakaryocytic, and erythroid) present in the bone marrow, including peripheral blood progenitor stem cells; for seven of the eight patients carrying the translocation, it was found in 96%-100% of the unfractionated bone marrow cells as well as in all of the FACS-purified cell fractions in which it could be detected or studied. Conventional cytogenetic analyses performed on representative bone marrow aspirates confirmed the results obtained by FISH analysis. Cells in control bone marrow samples obtained from the five healthy donors were negative for the t(14;18) translocation by FISH analysis. CONCLUSIONS: Our findings indicate that the t(14;18) translocation most probably occurs in a very early multilineage progenitor stem cell. IMPLICATIONS: Given that the t(14;18) chromosomal translocation was found in all types of bone marrow cells when only the B cells were malignant, our results suggest that this translocation is not sufficient to induce neoplastic transformation. This finding underscores the need for the development of new approaches for the detection and surveillance of B-NHL.

Chromosomes, Human, Pair 14↗
PubMed1992

Immunoglobulin-containing cells in chick embryo urogenital tissues: a new site for early B lineage cells in endothermic vertebrates.

We have employed histological and immunofluorescent staining procedures in order to characterize the distribution of mu + B lineage cells in tissue sections prepared from developing chicken embryo urogenital tissues (UGTs) between 14 and 21 days of incubation. B lineage cells were observed in tissue sections prepared from developing UGTs, especially the mesonephros and its associated tissue, throughout the sample period. The highest densities of mu + B lineage cells were observed in tissue sections prepared from 18 day embryos. The mu + UGT cells were distributed singly and in clusters in subcapsular regions and within the peritubular interstitium of the mesonephros. These observations (1) are consistent with those which suggest nonbursal site(s) for origin of cells in B lineage, (2) may help account for the varying effects of embryonic caudectomy performed between the second and third days of incubation and surgical bursectomy performed close to hatching, (3) may help provide new insights on the effects of sex hormones on B cell development, and (4) suggest fundamental ontogenetic and phylogenetic similarities between developing vertebrate immune systems.

Animals↗
PubMed1992

Sequential maturation stages of monoclonal B lineage cells from blood, spleen, lymph node, and bone marrow from a terminal myeloma patient.

In order to fully understand the complexity of the monoclonal B lineage cells in multiple myeloma, it is necessary to evaluate the extent to which these cells are resident in solid lymphoid tissues and the phenotypic differences and similarities as compared to the circulating or bone marrow derived B lineage cells. Peripheral blood mononuclear cells from a patient with multiple myeloma were obtained 8 and 3 days prior to death, and mononuclear cells from lymph nodes, spleen, and bone marrow were obtained at autopsy. Rapid changes in the stage of differentiation of blood late-stage B lineage cells towards mature end-stage plasma cells were observed during the last week prior to death. Lymphoid cells within the blood comprised very few T cells, sub-normal numbers of monocytes, and 80% of B lineage cells which were at a late stage of differentiation. Shortly before death, plasma cells were found in the peripheral blood, indicating progression to plasma cell leukemia. At autopsy, the monoclonal B lineage cells in lymph node, spleen, and bone marrow represented different stages of terminal B cell differentiation. In each tissue, the B lineage cells were at an earlier differentiation stage, as defined phenotypically, than the circulating B lineage cells found in blood 3 days prior to death. Analysis of B cell markers and CD45 was used to define the differentiation stage of the relevant B cell populations, revealing a series of differentiation stages. The least mature B lineage cells (CD45hi) were found in lymph node. However, the CD45 isoform expressed was CD45R0, unlike most normal lymph node B cells. More differentiated B lineage cells (CD45med) were found in the bone marrow, and three sequential stages of pre-plasma cells were found in the spleen (CD45bright, CD45moderate, and CD45low-neg), all of which were CD45R0+. The B cells in normal spleen and bone marrow are CD45RA+. The presence of monoclonal B lineage cells in spleen was confirmed by Southern blotting. The B lineage cells from peripheral blood 3 days prior to death were approaching an end-stage plasma cell stage (CD45low/-). On B lineage cells from the various myeloma tissues, a concomitant loss of CD11b and increasing density of CD29 were observed as a function of progression to terminally differentiated stages.

Antibodies, Monoclonal↗
PubMed1993

A CNS-specific POU transcription factor, Brn-2, is required for establishing mammalian neural cell lineages.

The pluripotent embryonal carcinoma cell line P19 can differentiate in vitro into neurons and astrocytes. By employing this neural cell differentiation system, we have studied the expression and function of a POU transcription factor implicated in mammalian neurogenesis. When P19 cells differentiated to the neural cells, one of the CNS-specific POU genes (Brn-2) was selectively induced. The induction of Brn-2 was specific to the neural cell lineages and took place at the early stage of differentiation. When the Brn-2 induction was blocked/delayed by antisense RNA, such cells were unable to differentiate to neurons and astrocytes. Instead they differentiated to nonneural cells, including smooth and skeletal muscle cells. Furthermore, with reduced levels of antisense RNA, differentiation to neural cells occurred. These results indicate that Brn-2 is essential for the neural cell differentiation of P19 cells and suggest that Brn-2 is one of the genes required for establishing neural cell lineages in mammals.

Animals↗
PubMed2003

ALES: cell lineage analysis and mapping of developmental events.

MOTIVATION: Animals build their bodies by altering the fates of cells. The way in which they do so is reflected in the topology of cell lineages and the fates of terminal cells. Cell lineages should, therefore, contain information about the molecular events that determined them. Here we introduce new tools for visualizing, manipulating, and extracting the information contained in cell lineages. Our tools enable us to analyze very large cell lineages, where previously analyses have only been carried out on cell lineages no larger than a few dozen cells. RESULTS: Ales (A Lineage Evaluation System) allows the display, evaluation and comparison of cell lineages with the aim of identifying molecular and cellular events underlying development. Ales introduces a series of algorithms that locate putative developmental events. The distribution of these predicted events can then be compared to gene expression patterns or other cellular characteristics. In addition, artificial lineages can be generated, or existing lineages modified, according to a range of models, in order to test hypotheses about lineage evolution. AVAILABILITY: The program can run on any operating system with a compliant Java 2 environment. Ales is free for academic use and can be downloaded from http://mbi.dkfz-heidelberg.de/mbi/research/cellsim/ales.

Algorithms↗
PubMed1994

Embryonic fat-cell lineage in Drosophila melanogaster.

The Drosophila adipose tissue, or fat body, and the bodywall muscle are two major tissues derived from the mesoderm. Although much is known about the lineage of muscle cells, little is known about the development of the fat body. Using known genes and an enhancer trap (29D), we have begun to trace the lineage of the cells comprising the fat body. The genes Adh (alcohol dehydrogenase) and DCg1 (type IV collagen) code for gene products involved in fat-cell metabolism and therefore serve as terminal fat-cell differentiation markers. The expression of these genes was used to identify the fat body at stage 17 and to identify the start of terminal fat-cell differentiation at stage 15. We found that the steroid-hormone receptor gene, svp (seven-up), was expressed transiently within the fat-cell lineage from stages 12 to 14. We suggest that stage 12 marks the beginning of early fat-cell differentiation and that the svp-positive cells within the mesoderm are early precursor fat cells. To confirm the identity of these cells and to establish the role of svp in the developing fat cell, we examined svp mutant embryos for alterations in the expression of the two terminal fat-cell differentiation markers, Adh and DCg1. Loss of svp function resulted in the loss of Adh transcript and a reduction of DCg1 expression specifically in the fat body. Thus, svp plays a role in fat-body-specific expression of at least two terminal fat-cell differentiation genes. In contrast to svp, we found no evidence that the steroid receptor HNF-4(D) gene was expressed in the fat body nor that it was involved in the development of this tissue. Using an enhancer-trap line (29D), we further traced the fat-cell lineage to nine bilateral clusters of cells within the mesoderm at germ-band extension. We suggest these 29D-positive cells represent the progenitor fat cells. In stage-12 embryos, the 29D-positive cell clusters can be identified within the mesoderm internal to nautilus-expressing cells. These data suggest that the precursor fat cells may be derived from the inner mesoderm, or spanchnopleura. Embryos deficient for the DNA region surrounding the site of the 29D enhancer trap lack most, if not all, of the cells in the fat-cell lineage. These embryos exhibit the loss of svp-positive precursor fat cells and concomitant loss of fat-body-specific expression of Adh and DCg1.(ABSTRACT TRUNCATED AT 400 WORDS)

Alcohol Dehydrogenase↗
PubMed2001

Two types of asymmetric divisions in the Drosophila sensory organ precursor cell lineage.

Asymmetric partitioning of cell-fate determinants during development requires coordinating the positioning of these determinants with orientation of the mitotic spindle. In the Drosophila peripheral nervous system, sensory organ progenitor cells (SOPs) undergo several rounds of division to produce five cells that give rise to a complete sensory organ. Here we have observed the asymmetric divisions that give rise to these cells in the developing pupae using green fluorescent protein fusion proteins. We find that spindle orientation and determinant localization are tightly coordinated at each division. Furthermore, we find that two types of asymmetric divisions exist within the sensory organ precursor cell lineage: the anterior-posterior pI cell-type division, where the spindle remains symmetric throughout mitosis, and the strikingly neuroblast-like apical-basal division of the pIIb cell, where the spindle exhibits a strong asymmetry at anaphase. In both these divisions, the spindle reorientates to position itself perpendicular to the region of the cortex containing the determinant. On the basis of these observations, we propose that two distinct mechanisms for controlling asymmetric cell divisions occur within the same lineage in the developing peripheral nervous system in Drosophila.

Animals↗
PubMed1990

Primary treatment of childhood acute lymphoblastic leukemia of non-T cell lineage (including infants).

About 85% of children with ALL have leukemic blasts that express cell membrane antigens associated with B-cell lineage, although few are surface immunoglobulin positive. Patients differ from children with ALL of T-cell lineage in that they tend to be younger, less predominantly male, and less likely to have a mediastinal mass or CNS leukemia at diagnosis, and they have a lower leukocyte count. Leukemic blasts from these children are more likely to be hyperdiploid. However, B cell-lineage ALL is not homogeneous either. It includes infants, children, and adolescents; it includes patients with leukemic blasts that either express or fail to express CD10, CD24, and cytoplasmic immunoglobulin. B cell-lineage ALL includes patients with blasts showing hyperdiploidy and patients with blasts with translocations such as t(4;11), t(1;19), and t(9;22). In general, outcome for patients with B cell-lineage ALL is superior to the outcome of those with T cell-lineage ALL in univariate analysis. However, when comparisons are stratified by age and leukocyte count, any apparent prognostic advantage for children with B cell-lineage ALL is diminished. The addition of effective CNS prophylaxis to effective systemic chemotherapy made cure a reality for about one half of children with ALL. Subsequent work has made it possible to omit cranial irradiation and its sequelae for most children with ALL. At least three regimens have offered an unambiguous improvement over the original St. Jude prophylactic CNS therapy regimen. These regimens are the BFM 76/79 regimen, the New York regimen, and the Dana-Farber regimen. Cure appears possible for 70% of children. These regimens differ markedly in detail, but appear to benefit similar subsets of patients. Identification of their critical therapeutic elements is one challenge for the future. A second challenge is the early identification of patients likely to do poorly on these effective regimens, whether by age under 1 year, specific blast morphology, cytochemical findings, immunophenotype, cytogenetic findings, drug pharmacokinetic features, or early response to antileukemic therapy. The third challenge is continued awareness of the acute morbidity of therapy and its impact on the lives of children and their families, together with a heightened vigilance for likely long-term sequelae. Most children with lymphoblastic leukemia in the United States are referred to cancer treatment centers for the initiation of therapy. Over one half of the children who are diagnosed participate in formal clinical trials.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed2005

Initial T cell frequency dictates memory CD8+ T cell lineage commitment.

Memory T cells can be divided into central memory T cell (T(CM) cell) and effector memory T cell (T(EM) cell) subsets based on homing characteristics and effector functions. Whether T(EM) and T(CM) cells represent interconnected or distinct lineages is unclear, although the present paradigm suggests that T(EM) and T(CM) cells follow a linear differentiation pathway from naive T cells to effector T cells to T(EM) cells to T(CM) cells. We show here that naive T cell precursor frequency profoundly influenced the pathway along which CD8+ memory T cells developed. At low precursor frequency, those T(EM) cells generated represented a stable cell lineage that failed to further differentiate into T(CM) cells. These findings do not adhere to the present dogma regarding memory T cell generation and provide a means for identifying factors controlling memory T cell lineage commitment.

Animals↗
PubMed1991

NZB serum factor (NZB-SF)-B precursor cell maturation factor. II. In vivo effects of NZB-SF or mAb against NZB-SF on B lineage cell populations.

In vivo effects of NZB serum factor (NZB-SF), which enhances the maturation of B precursor cells in vitro, were examined. Immunoaffinity-purified NZB-SF from young NZB mice was injected into B6 mice intraperitoneally twice weekly, five times total (5 micrograms/dose/mouse). Control mice were given 0.01% albumin. Then the B lineage cell populations defined phenotypically (sIg+ cells, B220+ cells, and AA4.1+ cells) or the numbers of colony-forming B lineage cells were examined. NZB-SF-treated B6 mice exhibited a decrease in the percentage of B precursor cells in marrow, even though the percentage of sIg+ cells in marrow or spleen did not differ from controls. In contrast, the frequency of colony-forming B cells in marrow and spleen, especially sIg- colony-forming B cells in marrow, increased significantly in NZB-SF-treated mice as compared to controls. In addition, monoclonal antibody (mAb) against NZB-SF was injected weekly for 9 weeks into NZB mice beginning at 7 weeks of age. mAb vs NZB-SF at a dose of 5 micrograms per mouse per injection, as stated above, prevented the decline of sIg- colony-forming B lineage cells which usually occurred in the adult NZB mice (greater than 16 weeks). This treatment also prevented, in part, the decline of the B220+ cell population which normally occurs in the marrow with increasing age. Thus NZB-SF impressively influences the composition of B lineage cell populations in normal B6 mice and may account for abnormal changes of B lineage cell populations observed in NZB mice.

Animals↗
PubMed2000

Notch-1 and Notch-2 exhibit unique patterns of expression in human B-lineage cells.

The Notch genes encode a conserved family of receptors that influence developmental fate in many species. Prior studies have indicated that Notch-1 and Notch-2 signaling influence the development of hematopoietic stems cells and thymocytes, but little is known regarding Notch expression and function in B-lineage cells. We analyzed the expression of Notch receptors and Notch ligands in human B-lineage cells and bone marrow (BM) stromal cells. Notch-1 mRNA and protein is expressed throughout normal B cell development and in leukemic B-lineage cells. In contrast, Notch-2 expression is limited to pre-B cells expressing low levels of surface mu. The Notch ligand Delta is expressed in BM B-lineage cells. The Notch ligand Jagged-1 is not expressed in B-lineage cells, but is expressed in BM stromal cells. These results suggest a model wherein lateral signaling between Notch and Delta on B-lineage cells and/or Notch/Jagged-1 interactions between B-lineage cells and BM stromal cells may regulate human B cell development.

Animals↗