IgG anti-tetanus toxoid antibody synthesis by human bone marrow. I. Two distinct populations of marrow B cells and functional differences between marrow and peripheral blood B cells

1990 ◽  
Vol 10 (5) ◽  
pp. 255-264 ◽  
Author(s):  
Lawrence G. Lum ◽  
Edith Burns ◽  
Marleen M. Janson ◽  
Paul J. Martin ◽  
Bernadette R. Giddings ◽  
...  
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Tetanus Toxoid ◽  
Peripheral Blood ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Antibody Synthesis ◽  
Functional Differences

scholarly journals A comparative analysis of human bone marrow–resident and peripheral memory B cells

2018 ◽  
Vol 141 (5) ◽  
pp. 1911-1913.e7 ◽  
Author(s):  
Sonya C. Becker ◽  
Martin Szyska ◽  
Angela Mensen ◽  
Katharina Hellwig ◽  
Raik Otto ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Comparative Analysis ◽  
B Cells ◽  
Memory B Cells ◽  
Human Bone ◽  
Human Bone Marrow

CCR5-binding chemokines modulate CXCL12 (SDF-1)–induced responses of progenitor B cells in human bone marrow through heterologous desensitization of the CXCR4 chemokine receptor

Blood ◽  
2002 ◽  
Vol 100 (7) ◽  
pp. 2321-2329 ◽  
Author(s):  
Marek Honczarenko ◽  
Yi Le ◽  
Aleksandra M. Glodek ◽  
Marcin Majka ◽  
James J. Campbell ◽  
...  
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
B Cell ◽  
Chemokine Receptor ◽  
Calcium Mobilization ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Cell Populations ◽  
B Lymphopoiesis ◽  
Heterologous Desensitization

Although the SDF-1 (CXCL12)/CXCR4 axis is important for B-cell development, it is not yet clear to what extent CC chemokines might influence B lymphopoiesis. In the current study, we characterized CC chemokine receptor 5 (CCR5) expression and function of primary progenitor B-cell populations in human bone marrow. CCR5 was expressed on all bone marrow B cells at levels between 150 and 200 molecules per cell. Stimulation of bone marrow B cells with the CCR5-binding chemokine macrophage inflammatory protein 1β (MIP-1β; CCL4) did not cause chemotaxis, but CCL4 was able to trigger potent calcium mobilization responses and activation of the mitogen-activated protein kinase (MAPK) pathway in developing B cells. We also determined that CCR5-binding chemokines MIP-1α (CCL3), CCL4, and RANTES (CCL5), specifically by signaling through CCR5, could affect all progenitor B-cell populations through a novel mechanism involving heterologous desensitization of CXCR4. This cross-desensitization of CXCR4 was manifested by the inhibition of CXCL12-induced calcium mobilization, MAPK activation, and chemotaxis. These findings indicate that CCR5 can indeed mediate biologic responses of bone marrow B cells, even though these cell populations express low levels of CCR5 on their cell surface. Thus, by modulation of CXCR4 function, signaling through CCR5 may influence B lymphopoiesis by affecting the migration and maturation of B-cell progenitors in the bone marrow microenvironment.

scholarly journals Expression of the YB5.B8 antigen (c-kit proto-oncogene product) in normal human bone marrow

Blood ◽  
1991 ◽  
Vol 78 (1) ◽  
pp. 30-37 ◽  
Author(s):  
LK Ashman ◽  
AC Cambareri ◽  
LB To ◽  
RJ Levinsky ◽  
CA Juttner
Keyword(s):  
Bone Marrow ◽  
Peripheral Blood ◽  
Bone Marrow Cells ◽  
Lymphoid Cells ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Hematopoietic Stem ◽  
Normal Peripheral Blood ◽  
Normal Human ◽  
Normal Human Bone Marrow

Abstract The c-kit proto-oncogene product is a member of the family of growth factor receptors with intrinsic tyrosine kinase activity. In the mouse c-kit maps to the W locus, which is known to be of central importance in hematopoiesis. Monoclonal antibody (MoAb) YB5.B8, which was raised against peripheral blood blast cells from a patient with acute myeloid leukemia (AML), was recently shown to bind to the extracellular domain of the c-kit product. This antibody does not bind detectably to normal peripheral blood cells and identifies a sub-group of AML patients with poor prognosis. We have used MoAb YB5.B8 to study the expression of c- kit by normal human bone marrow cells by immunofluorescence and flow cytometry, and to isolate multipotential and erythroid colony-forming cells. In a series of 11 normal adult bone marrow specimens, MoAb YB5.B8 bound to 4.0% +/- 1.8% of the cells in the low-density fraction. Dual-labeling experiments were performed with YB5.B8, and CD33, CD34, and CD10 MoAbs. Three populations of cells binding YB5.B8 could be identified based on their pattern of coexpression of the other markers; ie, YB5.B8+/CD34+/CD33-, YB5.B8+/CD34+/CD33+ and YB5.B8+/CD34+/CD33+. These populations had distinctive two-dimensional light scatter characteristics and are likely to correspond to precursor colony- forming cells, colony-forming cells, and maturing mast cells, respectively. No cells binding both YB5.B8 and an MoAb to the early lymphoid marker CD10 were found, implying that most early lymphoid cells do not express c-kit. MoAbs to the c-kit protein should prove valuable in multimarker studies of human hematopoietic stem and progenitor cells. Definition of a reference range of c-kit expression in normal human bone marrow will provide a sound basis for further studies of this marker in diagnosis and prognosis in AML.

Characterisation of Side Population (SP) Cells Obtained from Different Hematopoietic Progenitor/Stem Cell Compartments in Human Bone Marrow and Peripheral Blood.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4170-4170
Author(s):  
Dag Josefsen ◽  
Lise Forfang ◽  
Marianne Dyrhaug ◽  
Gunnar Kvalheim
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Cell Population ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Hematopoietic Stem ◽  
Cell Compartments ◽  
Cd34 Cells

Abstract Side population (SP) cells are characterised by their ability to exclude Hoechst 33342 dye from the cells. Using this method, it has been demonstrated that cells within the SP+ fraction of mononuclear cells from both murine and human hematopoietic systems are enriched for primitive hematopoietic stem- and progenitor cells. Moreover, most of the SP+ cells did not express CD34, indicating the presence of a CD34 negative hematopoietic stem cell population. To explore this further, we have examined SP+ cells obtained from different cell compartments in human bone marrow and peripheral blood. Human bone marrow (BM) was obtained from healthy volunteer donors by iliac crest aspiration after informed consent. Mononuclear cells (MNC) were obtained by Ficoll grade centrifugation. CD34+ cells were then isolated from MNC. Highly enriched CD34+ cells were isolated from PBPC obtained from patients with Hodgkin lymphoma. To identify the SP+ cells, the cells were stained with Hoechst 33342 dye. Using flowcytometric techniques (FACStar+, FACSDiva, Becton Dickinson, San Jose, CA) we were able to visualize the dye efflux in SP+ cells. SP+ cells were functionally confirmed using Verapamil. Phenotypical characterisation of the different cell populations using flow cytometric methods was performed. The level of SP+ cells in BM-MNC was 1,3% (mean, n=3) In line with previous findings, we observed that SP+ cells obtained from BM-MNC lack expression of several lineage committed markers, including CD15 and CD19. Most of the cells were CD34− (mean=2,2%), which was lower than in the main population (MP; mean=5%). The level of CD133 expression was low and similar in both populations. Furthermore we found a higher fraction of CD3+ T-cells in the SP fraction than in the MP fraction (mean: 69% vs 51%). To further investigate the SP+CD34+ cell fraction, we examined CD34+ cells isolated from both human bone marrow and peripheral blood. The percentage of SP+CD34+ cells varied from 0,4 up to 18% of the total CD34+ cell population obtained from PBPC (n= 16), whereas the level of SP+CD34+ cells obtained from bone marrow was 5% of the total CD34+ cell population (n=3). Expression of lineage committed markers, including CD10, CD15 and CD19 was less then 10% of the whole CD34+ cell population obtained from PBPC, whereas we found a higher level of expression of these markers in CD34+ cells isolated from bone marrow. However, when we examined the SP+CD34+ cells from either PBPC or bone marrow, we observed that the phenotypic profile of these cells were similar with almost no expression of lineage markers. The frequency of LTC-IC was markedly increased in SP+MNC, in line with previous findings. In addition we also observed a marked increase in LTC-IC in SP+CD34+ cells compared to SP-CD34+ cells in both BM and PB (BM: 7-fold increase; PB: 3–4 fold). In conclusion, SP cells are present in different hematopoietic progenitor cell populations, including BM-MNC, BM-CD34+ cells and PB-CD34+ cells. In SP+CD34+ cell fractions from both BM and PB we observed an increased expression of stem cell markers like CD90 and CD133, whereas in SP+MNC we found low levels of CD34, CD90 and CD133 expression. However, the LTC-IC frequency was markedly higher in all SP+fractions compared to MP fractions, suggesting that sorting of SP+ cells from different hematopoietic stem- and progenitor cell compartments identify immature hematopoietic cells.

Glucocorticoid-Induced Apoptosis in Early B Cells from Human Bone Marrow

2002 ◽  
Vol 227 (9) ◽  
pp. 763-770 ◽  
Author(s):  
Deborah Lill-Elghanian ◽  
Kenneth Schwartz ◽  
Louis King ◽  
Pam Fraker
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Initial Population ◽  
In Vitro Response ◽  
B Lineage ◽  
Induced Apoptosis ◽  
High Degree

The sensitivity of normal human lymphoid precursor cells to glucocorticoid-induced apoptosis is a subject of controversy. The in vitro response of cells of the B lineage (CD19+) from the marrow of 22 adult subjects to glucocorticoids was evaluated herein using both natural steroids and dexamethasone (Dex). When exposed to 1 μM Dex, 32% of the subjects exhibited high losses of CD19+ B cells in the range of 45%. The remaining subjects exhibited more modest losses in CD19+ cells of 26%–40%. Surprisingly, cortisol, a naturally produced glucocorticoid, produced B lineage losses nearly equivalent to Dex, which reached maximum by 12 hr. It was subsequently noted that the variances in losses of CD19+ cells among the subjects correlated closely with the proportion of early CD10+ CD19+ B cells present in the initial population. The latter cells exhibited a high degree of sensitivity to glucocorticoids, with losses of 60%–80% noted. Mature B cells bearing IgD, on the other hand, were fairly resistant to glucocorticoids. Merocyanine 540, a membrane dye that fluoresces in the disordered membrane of apoptotic cells, confirmed that early or progenitor B cells in human bone marrow were indeed undergoing glucocorticoid-induced apoptosis, which could be blocked by the glucocorticoid antagonist RU38486. These data provide evidence that human marrow B cells, especially early B-cell progenitors, are quite sensitive to glucocorticoids and readily undergo apoptosis within a few hours of exposure to the steroids.

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