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Results for “Cell Lineage”

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PubMed2000

Low expression level but potent antigen presenting function of CD1d on monocyte lineage cells.

CD1d is a key antigen-presenting molecule involved in the selection and activation of a highly conserved T cell subset known as NK T cells. In this study, we analyzed the expression, regulation and function of human CD1d by various antigen-presenting cells (APC) of myeloid origin, including circulating monocytes, monocyte-derived dendritic cells and macrophages. CD1d was expressed as a mature glycoprotein by these cells, and unlike the other members of the human CD1 family its expression was constitutive and was not strongly up-regulated by GM-CSF and IL-4 or a range of other cytokines. Despite their remarkably low surface expression of CD1d, all myeloid lineage cells tested were extremely potent APC for responses of NK T cell clones to the synthetic glycolipid antigen, alpha-galactosyl ceramide. Prominent localization of CD1d to the endocytic system of monocyte lineage cells was observed, and functional studies suggested that this was important for achieving efficient antigen loading onto CD1d. Overall, these results support the view that monocyte lineage cells are important stimulators of CD1d-restricted immune responses, while also underscoring the unique regulation of CD1d expression by these cells.

Antibodies, Monoclonal↗

PubMed1988

Prostaglandin E2-mediated inactivation of various killer lineage cells by tumor-bearing host macrophages.

We have previously reported that natural killer (NK) lineage cells are progressively inactivated during tumor development by prostaglandin E2 (PGE2) secreted by host macrophages; that this facilitates spontaneous tumor metastases, which can be prevented by chronic indomethacin therapy (CIT); and that CIT combined with multiple rounds of interleukin 2 (IL-2) can cure experimental metastases and activate all killer lineage cells in situ including NK cells, lymphokine-activated killer (LAK) cells, and tumoricidal macrophages. The present study tested whether PGE2 secreted by tumor-bearing host macrophages exerts pansuppressor effects against the activation of T cells, NK cells, LAK cells, and tumoricidal macrophages from normal splenic cell populations. Macrophages isolated from CBA mice bearing 21-day intraperitoneal Ehrlich ascites tumors (EAT) or C3H/HeJ mice bearing 21-day subcutaneous T58 mammary adenocarcinomas were added (+/- 10(-5) M indomethacin, or a monoclonal anti-PGE2 ab) to syngeneic splenic lymphocytes to examine the effects on 1) polyclonal activation (3-d 3H-thymidine [3H-TdR] uptake) with concanavalin A (Con A); 2) one-way (CBA alpha BALB/C or C3H alpha BALBC) MLR (5-d 3H-TdR uptake) and subsequent CTL generation (tested against 51Cr-labeled Con A blasts of the stimulator phenotype); 3) NK activity (after 24-h co-culture) against YAC-1 targets; 4) generation of LAK cell activity (in the presence of 200 or 2,000 units recombinant IL-2 for 3 or 5 days), tested against NK-sensitive and NK-resistant targets. Similar effects were also noted on the generation of tumoricidal activity in normal splenic macrophages cultured for 3 days in the presence of LPS. Normal splenic macrophages added under the same conditions served as controls. Effects of pure PGE2 or PGF2 alpha (10(-6) M) were also examined on these activation events. Results revealed that tumor-host-derived macrophages (but not normal macrophages) markedly suppressed all these activation events and this suppression was abrogated nearly totally by indomethacin and totally by anti-PGE2 ab, indicating its mediation by PGE2. This finding ran parallel with high levels of PGE2 production by tumor-host-derived but not normal splenic macrophages. Pure PGE2 but not PGF2 alpha mimicked these suppressor effects. While tumoricidal activity was generated in normal macrophages in the presence of LPS, IL-2, or IFN-gamma or their various combinations (which led to further augmentation), these agents required the presence of indomethacin to generate significant killer activity in tumor-host-derived macrophages. macrophages.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2002

Normal fate and altered function of the cardiac neural crest cell lineage in retinoic acid receptor mutant embryos.

Mouse embryos lacking the retinoic acid (RA) receptors RARalpha1 and RARbeta suffer from a failure to properly septate (divide) the early outflow tract of the heart into distinct aortic and pulmonary channels, a phenotype termed persistent truncus arteriosus. This phenotype is associated with a failure in the development of the cardiac neural crest cell lineage, which normally forms the aorticopulmonary septum. In this study, we examined the fate of the neural crest lineage in RARalpha1/RARbeta mutant embryos by crossing with the Wnt1-cre and conditional R26R alleles, which together constitute a genetic lineage marker for the neural crest. We find that the number, migration, and terminal fate of the cardiac neural crest is normal in mutant embryos; however, the specific function of these cells in forming the aorticopulmonary septum is impaired. We furthermore show that the neural crest cells themselves do not utilize retinoid receptors and do not respond to RA during this process, but rather that the phenotype is cell non-autonomous for the neural crest cell lineage. This suggests that an alternative tissue in the vicinity of the outflow tract of the heart responds directly to RA, and thereby induces or permits the neural crest cell lineage to initiate aorticopulmonary septation.

Animals↗

PubMed1990

Patterns of cell lineage in the cerebral cortex reveal evidence for developmental boundaries.

Experimental aggregation chimeric mice offer a perspective on cell lineage relationships that is complementary to that of prospective tracing methods such as dye injections or recombinant retroviruses. To create a lineage map of cerebral cortex, the position and genotype of cortical neurons in three-dimensional space were reconstructed with the aid of a computer-assisted mapping system. Chi-square statistical analyses indicate that the spatial distribution of cell lineages in the cerebral cortex is highly nonrandom. When individual dimensions are analyzed separately, a high degree of order is found in the spatial distribution of neuronal genotype ratios in the anterior-posterior dimension but not in the medial-lateral dimension. This suggests an arrangement of lineage-related neurons into "slabs" or "stripes" of cells that are organized in the plane perpendicular to the neuraxis. Additionally, a highly significant variation in genotype ratios was found in the radial dimension (i.e., among cortical cell layers). These data suggest the hypothesis that separate sets of progenitor cells give rise to the superficial and deep layers of cortex. Taken together, our data are consistent with a picture of the developing nervous system in which early developmental restrictions to cell mixing set up boundaries that may be of considerable developmental genetic importance.

Animals↗

PubMed2001

Context-dependent Pax-5 repression of a PU.1/NF-kappaB regulated reporter gene in B lineage cells.

Enhancers located in the 3' end of the locus in part regulate immunoglobulin heavy chain (IgH) gene expression. One of these enhancers, HS 1,2, is developmentally regulated by DNA binding proteins like NF-kappaB, Pax-5 and the protein complex NF-alphaP in B lineage cells. Here we report that NF-alphaP is the ets protein PU.1. A glutathione-S-transferase (GST)-pulldown assay demonstrated that PU.1 can physically interact with NF-kappaB in solution. Experiments in COS cells showed that PU.1 and NF-kappaB (p50/c-Rel) can activate transcription of an enhancer linked reporter gene. The paired domain protein Pax-5 has previously been shown to repress enhancer-dependent transcription. Additional co-transfection experiments revealed that PU.1/NF-kappaB dependent transcription could be repressed in a context dependent manner by Pax-5, but not by the paired domain of Pax-5. When the PU.1 binding site was substituted with a binding site for the ets-protein Elf-1, Pax-5 could no longer repress reporter gene activity. Our data indicate a model where Pax-5 mediated repression of the HS 1,2 enhancer requires the recruitment of a co-factor which is dependent on Pax-5/PU.1 but which cannot be recruited by Pax-5/Elf-1.

Animals↗

PubMed1993

Human natural killer cell committed thymocytes and their relation to the T cell lineage.

Recent studies have demonstrated that mature natural killer (NK) cells can be grown from human triple negative (TN; CD3-, CD4-, CD8-) thymocytes, suggesting that a common NK/T cell precursor exists within the thymus that can give rise to both NK cells and T cells under appropriate conditions. In the present study, we have investigated human fetal and postnatal thymus to determine whether NK cells and their precursors exist within this tissue and whether NK cells can be distinguished from T cell progenitors. Based on the surface expression of CD56 (an NK cell-associated antigen) and CD5 (a T cell-associated antigen), three phenotypically distinctive populations of TN thymocytes were identified. CD56+, CD5-; CD56-, CD5-, and CD56-, CD5+. The CD56+, CD5- population of TN thymocytes, although displaying a low cytolytic function against NK sensitive tumor cell targets, were similar in antigenic phenotype to fetal liver NK cells, gave rise to NK cell clones, and were unable to generate T cells in mouse fetal thymic organ cultures (mFTOC). This population of thymocytes represents a relatively mature population of lineage-committed NK cells. The CD56-, CD5- population of TN thymocytes were similar to thymic NK cells in antigenic phenotype and NK cell clonogenic potential. Clones derived from this population of TN thymocytes acquired CD56 surface expression and NK cell cytolytic function. CD56-, CD5- TN thymocytes thus contain a novel population of NK cell-committed precursors. The CD56-, CD5- population of TN thymocytes also contains a small percentage of CD34+ cells, which demonstrate no in vitro clonogenic potential, but possess T cell reconstituting capabilities in mFTOC. The majority of TN thymocytes do not express CD56, but coexpress CD34 and CD5. These CD56-, CD5+, CD34+ cells demonstrate no NK or T cell clonogenic potential, but are extremely efficient in repopulating mFTOC and differentiating into CD3+, CD4+, CD8+ T cells. The results of this investigation have identified NK cells and NK cell precursors in the human thymus and have shown that these cell types are unable to differentiate along the T cell lineage pathway. Thus, while a common NK/T cell progenitor likely exists, once committed to the NK cell lineage these cells no longer have the capacity to develop along the T cell developmental pathway.

Antigens, CD↗

PubMed2005

Chromosomal radiosensitivity in two cell lineages derived from clinically radiosensitive cancer patients.

PURPOSE: Despite its prominent contribution to cancer cure and palliation, around 1% to 5% of cancer patients suffer serious side effects from radiotherapy. A cardinal goal in the fields of radiobiology and oncology is to predict normal tissue radiosensitivity of a cancer patient before radiotherapy. Higher tumor control rates are likely if radiotherapy individualization could be achieved by applying predictive approaches. EXPERIMENTAL DESIGN: Here, we make use of the cytokinesis block micronucleus assay to assess radiosensitivity in cell lines derived from two different cell lineages obtained from clinically radiosensitive patients. We determined the micronucleus frequency after graded doses of ionizing radiation to primary fibroblasts and lymphoblast cell lines derived from 36 highly radiosensitive cancer patients. RESULTS: Many cell lines, following exposure to ionizing radiation, from patients with severe clinical reactions to radiotherapy showed statistically significantly higher frequencies of micronuclei than those from patients who had normal reactions to radiotherapy. One individual revealed significantly higher micronucleus frequencies in both cell lineages. Interestingly, lymphoblast cell lines from one patient showed micronucleus frequencies similar to ataxia telangiectasia mutated-deficient cells. CONCLUSIONS: These results indicate that the micronucleus assay may have use for identifying predisposition to clinical radiosensitivity, at least in a subset of patients as a component of a pretreatment radiosensitivity assay for use in the clinic.

Cell Lineage↗

PubMed2006

Developmental stages and germ cell lineage of the loach (Misgurnus anguillicaudatus).

The staging of embryonic and larval development, and the germ cell lineage of the loach, Misgurnus anguillicaudatus, are described. Fertilized eggs were obtained by artificial insemination. For the convenience of detailed observation and photography of the external appearance, we use dechorionated embryos. Through a series of operations, these embryos were cultured at 20 degrees C in an incubator. Embryonic and larval development of the loach was divided into five periods: cleavage, blastula, gastrula, segmentation, and hatching. Stages were assigned within each of these periods. Developmental stages were determined and named by morphological features and somite number. The staging series were photographed and tabulated. The germ cell lineage was then elucidated by whole mount in situ hybridization of mRNA expression of the germ-cell-specific marker vasa and histological analysis. Primordial germ cells (PGCs) of the loach derived from the cleavage furrows of 8-cell stage embryos began proliferation in the late blastula period and migrated to the gonadal anlagen through a migration pathway similar to that of the zebrafish. However, it is characteristic of the loach that PGCs migrate a long distance and stay in the posterior part of the yolk-extension region.

Animals↗

PubMed1993

Ulcer-associated cell lineage ('pyloric metaplasia') in Crohn's disease: a lectin histochemical study.

Chronic intestinal ulceration in Crohn's disease is associated with the development of an epidermal growth factor-secreting cell lineage, or 'ulcer-associated cell lineage' (UACL). Expression of oligosaccharides by UACL was studied using a panel of 25 biotinylated lectins with an avidin peroxidase revealing system and compared with that of adult and fetal Brunner's glands, gastric antral mucosa, and 'gastric metaplasia' within the duodenum, in order to clarify further the interrelationships of these lineages. UACL was obtained from ileal resections performed for Crohn's disease. Lectin binding of the glandular component of UACL closely resembled that of antral mucosal glands and also that of fetal and adult Brunner's glands. Lectin binding of the ductal component of immature UACL, in which a surface component had not developed, resembled that of the gland. The surface and ductal components of mature UACL showed a distinct lectin-binding profile, which was very different from that of the gland, but closely resembled that of antral foveolar epithelium and 'gastric metaplasia' within the duodenum. It is concluded that there is differentiation of UACL from the glandular to surface components and that oligosaccharide expression of the lineage reflects that of normal Brunner's gland and gastric antral mucosa.

Brunner Glands↗

PubMed1994

Cell lineage of the prototroch of Patella vulgata (Gastropoda, Mollusca).

The trochophore larva of the archaeogastropod mollusc Patella vulgata has a well-developed locomotory organ, the ciliated prototroch. This structure is formed from specific founder cells, the trochoblasts. Two methods were employed to determine the composition and cell lineage of the prototroch. Fluorescent cell-lineage tracer injection in trochoblasts and trochoblast founder cells was used to show how the various trochoblasts became incorporated into the prototroch. Scanning electron microscopy was used to study both differentiation, more specifically ciliation, of trochoblasts and localization of trochoblasts in the prototroch. The results obtained with both methods are in accordance with each other. During early development all trochoblasts involved in prototroch formation become cell cycle-arrested and develop cilia. Subsequently, the trochoblasts shift in position to form a circular prototroch and a number of trochoblasts deciliate. As a result of these processes the mature prototroch consists of a number of heavily ciliated cells as well as a number of deciliated cells. Comparison of prototrochs from a number of spiralian species shows that this structure is very conserved during evolution. The significance of this is discussed.

Animals↗

PubMed1992

Role of ultrastructural studies in the analysis of cell lineage in the mammalian pre-implantation embryo.

Ultrastructural studies have contributed significantly to our understanding of cell lineage differentiation in the mammalian pre-implantation embryo. Such studies have documented, and continue to document, morphological, biochemical, and physiological characteristics of the cell lineages established during the pre-implantation period in eutherian embryos, principally that of the mouse. This review evaluates these contributions and identifies areas of study in which ultrastructural analysis is most likely to have an important role in the future.

Animals↗

PubMed2006

Activated Notch1 alters differentiation of embryonic stem cells into mesodermal cell lineages at multiple stages of development.

Signals of Notch transmembrane receptors function to regulate a wide variety of developmental cell fates. Here we investigate the role of Notch signaling in the development of mesodermal cell types by expressing a tamoxifen-inducible, activated form of Notch1 in embryonic stem cells (ESC). For differentiation of ESC into first mesodermal progenitor cells and then endothelial, mural, cardiac muscle and hematopoietic cells, the OP9 stroma co-culture system was used. Timed activation of Notch signaling by the addition of tamoxifen at various stages during differentiation of ESC into mesodermal cell lineages results in profound alterations in the generation of all of these cells. Differentiation of ESC into Flk1(+) mesodermal cells is inhibited by activated Notch. When Notch signaling is activated in mesodermal cells, generation of cardiac muscle, endothelial and hematopoietic cells is inhibited, favoring the generation of mural cells. Activation of Notch signaling in hematopoietic cells reduces colony formation and maintenance of hematopoiesis. These data suggest that Notch signaling plays a regulatory role in mesodermal development, cardiomyogenesis, the balanced generation of endothelial versus mural cells of blood vessels and hematopoietic development.

Cell Differentiation↗

PubMed1998

Flow cytometric diagnosis of the cell lineage and developmental stage of acute lymphoblastic leukemia by novel monoclonal antibodies specific to human pre-B-cell receptor.

Three novel monoclonal antibodies (MoAbs) have been established that recognize distinct epitopes of a human pre-B-cell receptor (pre-BCR) composed of a mu heavy (muH) chain and a lambda5/VpreB surrogate light (SL) chain. HSL11 reacts with lambda5 whereas HSL96 reacts with VpreB. Intriguingly, HSL2 does not bind to each component of the pre-BCR but does bind to the completely assembled pre-BCR complex. Flow cytometric analyses with cytoplasmic staining of a panel of human cell lines showed that HSL11 and HSL96 specifically stained cell lines derived from the pro-B and pre-B-cell stages of B-cell development. In contrast, HSL2 stained exclusively cell lines derived from the pre-B-cell stage. These results prompted us to explore the possibility of clinical application of these MoAbs for the determination of the cell lineage and developmental stage of acute lymphoblastic leukemia (ALL). Whereas none of mature B-lineage ALLs (B-ALLs), T-lineage ALLs (T-ALLs), and acute myeloid leukemias analyzed were stained in the cytoplasm with these three MoAbs, the vast majority of non-B- and non-T-ALLs (53 out of 56 cases) were found positive for either lambda5, Vpre-B, or both in their cytoplasm. Among these 53 cytoplasmic SL chain-positive ALLs, 19 cases were also positive for cytoplasmic muH chain, indicative of pre-B-cell origin. Interestingly, 6 out of these 19 pre-B-ALL cases were found negative for cytoplasmic staining with HSL2. From these results, we propose a novel classification of B-ALL in which five subtypes are defined on the basis of the differential expression of SL chain, muH chain, pre-BCR, and light chain along the B-cell development.

Antibodies, Monoclonal↗

PubMed1987

Leu-9 (CD 7) positivity in acute leukemias: a marker of T-cell lineage?

Monoclonal antibody Leu-9 (CD 7) has been reported to be a sensitive and specific marker for T-cell lineage in leukemic processes, since it is positive in patients whose leukemic cells fail to express other T-cell antigens. To test whether Leu-9 is indeed specific for T-cell leukemias, we examined in detail 10 cases of acute leukemia in which reactions were positive for Leu-9 and negative for other T-cell-associated markers including T-11, Leu-1, T-3, and E-rosettes. Morphologically and cytochemically, 2 of these 10 leukemias were classified as lymphoblastic, 4 as myeloblastic, 2 as monoblastic, 1 as megakaryoblastic, and 1 as undifferentiated. The case of acute megakaryoblastic leukemia is the first reported case to be Leu-9 positive. None of the 10 were TdT positive. Of six cases (two monoblastic, one lymphoblastic, one myeloblastic, one megakaryoblastic, and one undifferentiated) in which we evaluated for DNA gene rearrangements, only one, a peroxidase-positive leukemia, showed a novel band on study of the T-cell-receptor beta-chain gene. We therefore conclude that Leu-9 is not a specific marker to T-cell lineage and that, in the absence of other supporting data, Leu-9 positivity should not be used as the sole basis of classifying an acute leukemia as being T-cell derived.

Acute Disease↗

PubMed1998

Mechanism of catecholamine-mediated destabilization of messenger RNA encoding Thy-1 protein in T-lineage cells.

The Ig superfamily cell surface glycoprotein Thy-1 expressed on immune cells and neurons of rodents and humans is hypothesized to function in cell adhesion and signal transduction in T cell differentiation, proliferation, and apoptosis. This study analyzes effects of cAMP and catecholamines on transcriptional Thy-1 gene expression. Incubation of murine thymocytes or S49 mouse thymoma cells with dibutyryl-cAMP, 8-bromo-cAMP, cholera toxin, norepinephrine, or isoproterenol caused time- and concentration-dependent decreases in levels of Thy-1 mRNA assayed by Northern hybridization or T2 nuclease protection. After 4 h of treatment with 500 microM dibutyryl-cAMP or 8-bromo-cAMP, 1 nM cholera toxin, 100 microM norepinephrine, or 100 microM isoproterenol, Thy-1 mRNA levels were 60 to 96% lower than those of controls. Norepinephrine-mediated decreases in Thy-1 mRNA levels were prevented by the beta-adrenergic receptor antagonist propranolol (10 microM). Dibutyryl-cAMP and norepinephrine decreased the apparent half-life of S49 cell Thy-1 mRNA from >>6 h to 2 to 3 h, whereas nuclear run-on assays showed no cAMP or norepinephrine effect on de novo transcription of the Thy-1 gene. In mutant S49 cells lacking cAMP-dependent protein kinase A, neither dibutyryl cAMP nor norepinephrine affected Thy-1 mRNA levels. These observations show that exogenous cAMP and norepinephrine can induce decreases in steady state Thy-1 mRNA levels in T-lineage cells through posttranscriptional destabilization of Thy-1 mRNA, associated with protein kinase A-mediated protein phosphorylation. Catecholamine-mediated beta-adrenergic protein kinase A-dependent Thy-1 mRNA destabilization may be an example of a more general mRNA decay system regulating cellular responses to stress.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMedDate not supplied

Implanted bone particles induce osteoclast development in the presence of osteoblast lineage cells.

We implanted mineral-containing bone particles (BPs) in rats to investigate the involvement of osteoblast lineage cells in osteoclast development in vivo. BPs were implanted in subcutaneous regions on calvaria or artificial defects of calvaria, with or without adjacent parathyroid glands prepared from other rats. The structural characteristics of multinucleated giant cells (MGCs) induced by the BPs were investigated. The MGCs induced by subcutaneously implanted BPs showed membrane ruffling at the basolateral site, but not at the apical site, regardless of whether parathyroid glands were also implanted. In contrast, the MGCs induced by intraosseously implanted BPs showed the characteristics of osteoclasts, i.e., ruffled borders at the apical sites, clear zone, vacuoles, many mitochondria, and scattered rough endoplasmic reticulum. When BPs and parathyroid glands were implanted in bone defects, the number of MGCs was increased compared to that induced by BPs only. These MGCs showed the typical characteristics of active osteoclasts, including developed ruffled borders and stacks of Golgi succules. The number of osteoclasts was also investigated quantitatively by counting the numbers of MGCs positive and negative for tartrate-resistant acid phosphatase. In intraosseous implantation, MGCs with the characteristics of osteoclasts were observed close to osteoblastic cells characterized by developed rough endoplasmic reticulum. These results indicate that the osteoclasts were not induced solely by the subcutaneously implant BPs, but required osteoblast lineage cells for development.

Animals↗

PubMed2006

Growth of ameloblast-lineage cells in a three-dimensional Matrigel environment.

Enamel organ epithelial cells grow in culture as two distinct cell populations--either stellate-shaped or polygonal-shaped cells. The polygonal cells have an ameloblast cell phenotype and are difficult to grow in culture beyond two passages. This study was designed to determine the effects of a Matrigel three-dimensional (3D) environment on polygonal cells, as compared with stellate cells, derived from porcine tooth enamel organ. Enamel organs were dissected free from the unerupted molars of 30-kg pigs and then grown in LCH-8e media, either with or without serum. Cells grown in serum-free media were primarily polygonal shaped, whereas cells grown in media containing serum were stellate shaped. Both types of cells were grown in a 3D Matrigel matrix. In addition, polygonal-shaped cells were mixed with hydroxyapatite powder and transplanted subcutaneously into nude mice. Polygonal-shaped epithelial cells formed cell groups, similar to epithelial pearls, both in vitro and in vivo. The stellate-shaped cells, in contrast, did not form similar structures, but remained suspended in the Matrigel and gradually disappeared from the culture. These results suggest that a Matrigel environment, rich in basement membrane and matrix proteins, selects for polygonal-shaped ameloblast-lineage cells and induces the formation of epithelial pearls.

Ameloblasts↗

PubMed1983

Changes in B lineage cell population in liver and spleen of normal neonatal mice.

The frequency and characteristics of B lymphocyte lineage cells in neonatal murine liver and spleen were studied during the first 10 days after birth. These were distinguished as B cells with surface IgM (slgM), immediate precursors of B cells (pre-B cells) lacking slgM but containing micron-heavy chains of IgM, and earlier precursors that did not synthesize immunoglobulin but could be detected with monoclonal 14.8 antibody. Experiments were also done to relate these to cells capable of clonal proliferation in mitogen-containing semisolid agar cultures and cells that acquire this function only after preculture in liquid medium. Newborn liver contained large numbers of early precursors as well as pre-B cells, and culture studies revealed that a majority of the colony-forming B cells present at that time were slg-. Adherent accessory cells in newborn liver suspensions facilitated the maturation of these into functional B cells in vitro. At most ages, however, numbers of slg+ B cells detected in that tissue were surprisingly low. Possible explanations for this include a rapid exit of newly formed B cells and their immediate precursors from liver and/or a high rate of abortive lg gene rearrangements during the neonatal period. In contrast, whereas the spleen contained early precursors and pre-B cells at birth, these cells steadily declined in number with age as the numbers of slgM+ B cells increased. Adherent cells in liver but not spleen of immunodeficient CBA/N mice suppressed B lymphocyte formation in semisolid or liquid cultures. These observations document population dynamics in B lineage cells during a critical period of development.

Animals↗