Faculty Opinions recommendation of Cellular niches controlling B lymphocyte behavior within bone marrow during development.

2006 ◽  
Author(s):  
Timm Schroeder
Keyword(s):  
Bone Marrow ◽  
B Lymphocyte

scholarly journals A VCAM-like adhesion molecule on murine bone marrow stromal cells mediates binding of lymphocyte precursors in culture.

1991 ◽  
Vol 114 (3) ◽  
pp. 557-565 ◽  
Author(s):  
K Miyake ◽  
K Medina ◽  
K Ishihara ◽  
M Kimoto ◽  
R Auerbach ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Adhesion Molecule ◽  
Stromal Cells ◽  
Stromal Cell ◽  
Cell Adhesion Molecule ◽  
B Lymphocyte ◽  
Murine Bone Marrow

Two new mAbs (M/K-1 and M/K-2) define an adhesion molecule expressed on stromal cell clones derived from murine bone marrow. The protein is similar in size to a human endothelial cell adhesion molecule known as VCAM-1 or INCAM110. VCAM-1 is expressed on endothelial cells in inflammatory sites and recognized by the integrin VLA-4 expressed on lymphocytes and monocytes. The new stromal cell molecule is a candidate ligand for the VLA-4 expressed on immature B lineage lymphocytes and a possible homologue of human VCAM-1. We now report additional similarities in the distribution, structure, and function of these proteins. The M/K antibodies detected large cells in normal bone marrow, as well as rare cells in other tissues. The antigen was constitutively expressed and functioned as a cell adhesion molecule on cultured murine endothelial cells. It correlated with the presence of mRNA which hybridized to a human VCAM-1 cDNA probe. Partial NH2 terminal amino acid sequencing of the murine protein revealed similarities to VCAM-1 and attachment of human lymphoma cells to murine endothelial cell lines was inhibited by the M/K antibodies. All of these observations suggest that the murine and human cell adhesion proteins may be related. The antibodies selectively interfered with B lymphocyte formation when included in long term bone marrow cultures. Moreover, they caused rapid detachment of lymphocytes from the adherent layer when added to preestablished cultures. The VCAM-like cell adhesion molecule on stromal cells and VLA-4 on lymphocyte precursors may both be important for B lymphocyte formation.

scholarly journals Characterization of Incidentally Identified Minute Clonal B-Lymphocyte Populations in Peripheral Blood and Bone Marrow

2004 ◽  
Vol 122 (4) ◽  
pp. 588-595 ◽  
Author(s):  
Weina Chen ◽  
Sheryl L. Asplund ◽  
Robert W. McKenna ◽  
Steven H. Kroft
Keyword(s):  
Bone Marrow ◽  
Peripheral Blood ◽  
B Lymphocyte ◽  
Lymphocyte Populations

Constitutive overexpression of IL-5 induces extramedullary hematopoiesis in the spleen

Blood ◽  
2003 ◽  
Vol 101 (3) ◽  
pp. 863-868 ◽  
Author(s):  
Sophia Khaldoyanidi ◽  
Lyudmila Sikora ◽  
David H. Broide ◽  
Marc E. Rothenberg ◽  
P. Sriramarao
Keyword(s):  
Bone Marrow ◽  
Peripheral Blood ◽  
B Lymphocyte ◽  
Bone Marrow Cells ◽  
Extramedullary Hematopoiesis ◽  
Interleukin 5 ◽  
Bone Marrow Cultures ◽  
Constitutive Overexpression ◽  
Hematopoietic Activity

Abstract The differentiation of eosinophils from hematopoietic precursors and their subsequent maturation, chemotaxis, and activation is primarily regulated by interleukin-5 (IL-5). To examine the effect of chronic IL-5 exposure on hematopoiesis, IL-5 transgenic (IL-5trg) mice and wild-type BALB/c (WT) mice were examined. In comparison to WT mice, a significant alteration in bone marrow hematopoiesis was observed in IL-5trg mice. Although the total number of myeloid progenitors in the bone marrow of IL-5trg mice was not significantly altered, the number of long-term culture-initiating cells (LTC-ICs) was 1.5-fold lower than that observed in WT mice. Furthermore, IL-5trg mice failed to demonstrate hematopoietic activity in long-term bone marrow cultures, which correlated with a significant decrease in the number of bone marrow mesenchymal/stromal progenitor (MSP) cells in these mice. In comparison to WT mice, a 10-fold decrease was observed in the number of fibroblast colony-forming units (CFU-Fs) in IL-5trg bone marrow. Hematopoietic activity of IL-5trg bone marrow cells was rescued by cultivation on preestablished layers of bone marrow-derived stromal cells. However, in contrast to bone marrow, increased hematopoietic activity was observed in the spleen and peripheral blood of IL-5trg mice. Likewise, the numbers of LTC-ICs and granulocyte-macrophage, macrophage, eosinophil, B-lymphocyte progenitors in the peripheral blood and spleen of IL-5trg mice were approximately 20-fold higher than in WT mice. A significant increase in CFU-F numbers was also observed in the spleens of IL-5trg mice compared with WT mice. Overall, our results suggest that constitutive overexpression of IL-5 can potentially induce colonization of spleen with MSP cells, which provides the necessary microenvironment for establishment of hematopoiesis in extramedullary sites.

Clinical Consequences and Treatment of Primary Immunodeficiency Syndromes Characterized by Functional T and B Lymphocyte Anomalies (Combined Immune Deficiency)

PEDIATRICS ◽  
1994 ◽  
Vol 93 (2) ◽  
pp. 265-270 ◽  
Author(s):  
Françoise Berthet ◽  
Françoise Le Deist ◽  
Anne Marie Duliege ◽  
Claude Griscelli ◽  
Alan Fischer
Keyword(s):  
Immune Deficiency ◽  
Bone Marrow ◽  
Bone Marrow Transplantation ◽  
T Cell ◽  
Marrow Transplantation ◽  
B Lymphocyte ◽  
Severe Combined Immunodeficiency ◽  
Clinical Manifestations ◽  
Immunodeficiency Syndrome ◽  
Immunodeficiency Syndromes

Objective. To review the clinical presentation and outcome of patients with an unusual primary T + B lymphocyte immunodeficiency syndrome, characterized by the presence of T lymphocytes with no detectable gross phenotypic anomaly, but which are not activated in vitro or in vivo in response to antigens, although they do respond to mitogens. Methods. A retrospective analysis of clinical and immunological data recorded in 25 cases. Acquired immunodeficiencies and known primary T cell immunodeficiency syndromes (severe combined immunodeficiency syndrome, Di-George syndrome, Wiskott-Aldrich syndrome, cartilage hair hypoplasia, Omenn's syndrome, ataxia telangiectasia, defective expression of major histocompatability complex class II molecules, and defective expression of the CD3/T cell receptor complex) were excluded. Results. The patients had severe and particularly protracted infections, mainly of the respiratory tract and gut. Severe viral infections, generally due to herpes viruses, occurred in nearly two-thirds of the patients, with a median follow-up of 54 months. Autoimmune manifestations are frequent (60%), targetting mainly marrow-derived cells, and were characterized by a tendency to relapse and by a dependence on immunosuppressive therapy. Allergic manifestations were also frequent (48% of cases). Eight of the 19 patients who had not undergone bone marrow transplantation died. All but one of the 11 survivors had moderate to severe sequelae. Bone marrow transplantation seemed to be the treatment of choice, because four of six recipients of HLA-identical (n = 2) or nonidentical (n = 4) marrow are alive and the immune deficiency has been corrected. Conclusion. Early recognition of these life-threatening syndromes may improve the chances of cure. Despite common clinical manifestations and prognosis, these functional immunodeficiencies appear heterogeneous regarding inheritance pattern and at least existence of a B cell immunodeficiency.

Chronic lymphocytic leukaemia

2020 ◽  
pp. 5302-5310
Author(s):  
Clive S. Zent ◽  
Aaron Polliack
Keyword(s):  
Bone Marrow ◽  
Chronic Lymphocytic Leukaemia ◽  
B Cell ◽  
Peripheral Blood ◽  
B Lymphocyte ◽  
Lymphocytic Leukaemia ◽  
Bone Marrow Failure ◽  
Curative Therapy ◽  
Symptomatic Disease ◽  
Autoimmune Cytopenias

Chronic lymphocytic leukaemia (CLL)/small lymphocytic lymphoma is the most prevalent lymphoid neoplasm in Europe and North America. The ‘cell of origin’ is a mature B lymphocyte with a rearranged immunoglobulin gene. CLL cells express modest amounts of surface immunoglobulin, and are characterized by defective apoptosis. The cause of CLL is unknown. Most patients show no specific clinical features of disease and are diagnosed during evaluation of an incidental finding of peripheral blood lymphocytosis, lymphadenopathy, or splenomegaly. A small percentage of patients (<10%) present with symptomatic disease resulting from (1) tissue accumulation of lymphocytes such as disfiguring lymphadenopathy, splenomegaly with abdominal discomfort, profound fatigue, drenching night sweats, weight loss, and fever; or (2) manifestations of marrow failure with cytopenias including anaemia and thrombocytopenia. All CLL patients have an increased risk of infection, autoimmune cytopenias, and second haematological (e.g. diffuse large B-cell lymphoma) and nonhaematological malignancies. Diagnosis is usually made by analysis of the immunophenotype of the monoclonal circulating cells in the peripheral blood. In patients with the small lymphocytic variant of CLL without a detectable circulating monoclonal B-cell population, the diagnosis is made using tissue from the bone marrow, lymph nodes, or spleen. Treatment—there is no standard curative therapy and patients should not be treated until they have progressive and symptomatic disease or develop anaemia or thrombocytopenia due to bone marrow failure. If a decision is made to treat, then the best initial treatment should be given, based on evaluation of the patient’s disease characteristics with specific attention to the integrity of TP53 (coding for p53) and patient fitness.

scholarly journals Flow cytometric analysis of human bone marrow. II. Normal B lymphocyte development

Blood ◽  
1987 ◽  
Vol 70 (5) ◽  
pp. 1316-1324 ◽  
Author(s):  
MR Loken ◽  
VO Shah ◽  
KL Dattilio ◽  
CI Civin
Keyword(s):  
Bone Marrow ◽  
Cell Surface ◽  
B Lymphocyte ◽  
Human Bone ◽  
Lymphocyte Development ◽  
Hla Dq ◽  
B Lymphocyte Development ◽  
B Lineage ◽  
B Lymphoid ◽  
B Lineage Cells

Abstract A panel of B lymphoid-reactive monoclonal antibodies was used to analyze the phenotypic changes that accompany B lymphocyte development in normal human bone marrow. The B lymphoid cells were identified using light scattering and the expression of CD19 on a flow cytometer. Quantitative three-color immunofluorescence was then used to correlate other cell surface antigens on these cells identified as B lymphoid in normal marrow. CD10 and CD20 identified almost exclusive populations and provided a convenient means of discriminating between the less and more mature B lineage cells. The CD10+ cells could be further subdivided using CD34. The population of CD19+, CD10+, CD34+ cells comprised only 0.6% of marrow cells, but these contained the majority of terminal deoxynucleotidyl transferase (TdT+) cells. In the assessment of class II antigens, HLA-DR was expressed on all B lineage cells whereas HLA-DP preceded HLA-DQ in appearance during the developmental process. Among the later antigens expressed on B lineage cells, cell surface IgM, CD20, and HLA-DQ were expressed at essentially the same time. Cell surface CD10 was lost at the time when CD21 and CD22 were acquired on the cell surface. These data illustrate that multiparameter flow cytometry can be used to define a continuous progression of stages of B lymphocyte development based on cell surface antigen expression even though these cells represent a minor fraction of normal marrow cells.

scholarly journals B lymphocytes express and lose syndecan at specific stages of differentiation.

1989 ◽  
Vol 1 (1) ◽  
pp. 27-35 ◽  
Author(s):  
R D Sanderson ◽  
P Lalor ◽  
M Bernfield
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
B Cell ◽  
B Lymphocytes ◽  
B Lymphocyte ◽  
Plasma Cells ◽  
Receptor Expression ◽  
Cell Stage ◽  
Precursor B Cells

Lymphopoietic cells require interactions with bone marrow stroma for normal maturation and show changes in adhesion to matrix during their differentiation. Syndecan, a heparan sulfate-rich integral membrane proteoglycan, functions as a matrix receptor by binding cells to interstitial collagens, fibronectin, and thrombospondin. Therefore, we asked whether syndecan was present on the surface of lymphopoietic cells. In bone marrow, we find syndecan only on precursor B cells. Expression changes with pre-B cell maturation in the marrow and with B-lymphocyte differentiation to plasma cells in interstitial matrices. Syndecan on B cell precursors is more heterogeneous and slightly larger than on plasma cells. Syndecan 1) is lost immediately before maturation and release of B lymphocytes into the circulation, 2) is absent on circulating and peripheral B lymphocytes, and 3) is reexpressed upon their differentiation into immobilized plasma cells. Thus, syndecan is expressed only when and where B lymphocytes associate with extracellular matrix. These results indicate that B cells differentiating in vivo alter their matrix receptor expression and suggest a role for syndecan in B cell stage-specific adhesion.

scholarly journals B-lymphocyte heterogeneity: ontogenetic development and organ distribution of B-lymphocyte populations defined by their density of surface immunoglobulin.

1976 ◽  
Vol 144 (2) ◽  
pp. 494-506 ◽  
Author(s):  
I Scher ◽  
S O Sharrow ◽  
R Wistar ◽  
R Asofsky ◽  
W E Paul
Keyword(s):  
Bone Marrow ◽  
B Lymphocytes ◽  
B Lymphocyte ◽  
Bone Marrow Cells ◽  
Large Population ◽  
Organ Distribution ◽  
Spleen Cells ◽  
Adult Bone Marrow ◽  
Flow Microfluorometry ◽  
Adult Bone

The density of total Ig and of IgM, IgG1, IgG2, and IgA on the surface of adult murine splenic B lymphocytes was measured using the technique of rapid flow microfluorometry. In addition, the density of total surface Ig and of IgM on B lymphocytes derived from adult bone marrow, lymph nodes, and Peyer's patches, and from neonatal spleen was determined. Adult spleen and lymph node B lymphocytes are characterized by the presence of a large population of cells with a low-to-intermediate density of total surface Ig, which is seen as a peak in the fluorescence profiles when these cells are labeled with fluorescein-conjugated (F1) anti-Ig. This peak is not detected when neonatal spleen or adult bone marrow are examined; the development of this peak among spleen cells occurs during the first 4 wk of life. Although the characteristic fluorescence intensity peak is not seen when adult spleen cells are labeled with Fl anti-mu, changes in the density of surface IgM do occur during the first few weeks of life and are detected as a decrease in the frequency of cells which have relatively large amounts of surface IgM. The differences seen in the fluorescence patterns of adult spleen cells labeled with Fl anti-Ig and Fl anti-mu may be due to the appearance of IgD on the surface of mature splenic B lymphocytes. This is supported by the similarity of the fluorescence profiles of adult bone marrow cells stained with Fl anti-Ig and Fl anti-mu, as the latter population of cells is reported to lack surface IgD.

scholarly journals Maturation of bone marrow lymphocytes. II. Development of Fc and complement receptors and surface immunoglobulin studied by rosetting and radioautography.

1978 ◽  
Vol 148 (5) ◽  
pp. 1251-1270 ◽  
Author(s):  
W C Yang ◽  
S C Miller ◽  
D G Osmond
Keyword(s):  
Bone Marrow ◽  
B Lymphocyte ◽  
Bone Marrow Cells ◽  
Lymphoid Cells ◽  
Mouse Bone Marrow ◽  
Complement Receptors ◽  
Dna Labeling ◽  
Double Surface ◽  
B Lineage ◽  
Marrow Cells

Radioautographic DNA labeling and rosetting techniques were combined to study the development of surface IgM, Fc, and complement receptors (FcR, CR) on small lymphocyte populations in mouse bone marrow. [3H]thymidine was either infused continuously to label newly formed cells for periods up to 4 days, or injected daily, 21--35 days before use, to label a sample of long-lived cells. Bone marrow cells were incubated with sensitized sheep erythrocytes to detect surface IgM, FcR, and CR, respectively, and examined radioautographically after cytocentrifugation. During [3H]thymidine infusion, marrow small lymphocytes lacking surface markers were the first to show [3H]thymidine labeling. Most of these cells became labeled by 4 days (IgM--ve, 89%; FcR--ve, 92%; Cr--ve, 88%). Labeling of small lymphocytes bearing surface IgM, FcR, and Cr began after an initial lag and increased to high values by 4 days (IgM + ve, 73%; FcR + ve, 82%; CR + ve, 83%). Labeled IgM + ve small lymphocytes formed progressively larger rosettes as cell age increased. Some proliferating large lymphoid cells formed rosettes for IgM, FcR, and CR. Labeled long-lived small lymphocytes expressed surface IgM, FcR, and CR, the incidence of each receptor being uniformly high (38--43%) and the rosettes tending to be larger than those formed by newly formed lymphocytes. In double-surface marker studies, FcR and CR rosettes were formed by some IgM--ve small lymphocytes as well as IgM + ve cells in the marrow. After transfusion of marrow cells from donor mice infused with [3H]thymidine for 24 h, many labeled newly formed lymphocytes homed into the splenic red pulp of unlabeled syngeneic recipients. Subsequently, these cells showed a rapid increase in the incidence of rosettes for surface IgM, FcR, and CR, together with a progressive enlargement of each type of rosette. Although all the labeled small lymphocytes recovered from the spleen developed both surface IgM and FcR by 3 days, only approximately one-half developed CR. The results demonstrate that most of the small lymphocytes bearing FcR, CR, and surface IgM in mouse bone marrow are newly formed indigenous cells. Each receptor becomes detectable by rosetting soon after the small lymphocytes are first produced. The newly formed, marrow-derived small lymphocytes are able to continue their development of surface IgM, FcR, and CR after migrating into the spleen, consistent with a maturation of primary B lymphocytes. In addition, the data indicate the genesis in mouse marrow of a non-B lineage of lymphocytes (notably, IgM--ve FcR + ve cells.). A minority of small lymphocytes bearing IgM, FcR, and CR in mouse marrow are long-lived cells, presumptive recirculating immigrants, differing in receptor status from the newly formed cells. The results are discussed with regard to the heterogeneity of marrow lymphocytes and proposed models of primary B lymphocyte and null lymphocyte production.

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