Human interleukin 7 is a B cell growth factor for activated B cells

1991 ◽  
Vol 21 (3) ◽  
pp. 681-686 ◽  
Author(s):  
Pratibha C. Joshi ◽  
Yong Sung Choi
Keyword(s):  
B Cells ◽  
Growth Factor ◽  
Cell Growth ◽  
B Cell ◽  
Interleukin 7 ◽  
B Cell Growth Factor ◽  
Activated B Cells

scholarly journals The Bb fragment of complement factor B acts as a B cell growth factor.

1988 ◽  
Vol 168 (4) ◽  
pp. 1225-1235 ◽  
Author(s):  
M G Peters ◽  
J L Ambrus ◽  
A S Fauci ◽  
E J Brown
Keyword(s):  
B Cells ◽  
Growth Factor ◽  
Cell Growth ◽  
B Cell ◽  
Complement Factor ◽  
Factor B ◽  
Complement Factor B ◽  
B Cell Growth Factor ◽  
Cell Growth And Differentiation ◽  
Activated B Cells

The process of B cell growth and differentiation into plasma cells is highly regulated and may be influenced by a large number of inflammatory mediators, including complement components. We have studied the regulatory influence of Bb, a 60-kD peptide created during the cleavage of complement Factor B by Factor D and C3b. Purified Bb alone had no effect on proliferation and differentiation of human splenic or tonsillar B cells. However, when B cells were activated by Staphylococcus aureus Cowan I (SAC), Bb enhanced proliferation in a dose-dependent manner. Bb also enhanced proliferation when cocultured with SAC and suboptimal concentrations of purified 60-kD B cell growth factor (HMW-BCGF), a previously described lymphokine that is known to possess growth-promoting activity. However, Bb had no effect on cells treated with optimal concentrations of HMW-BCGF. Like HMW-BCGF, Bb's major effect was on the larger in vivo activated B cells. Half-maximal enhancement of proliferation was reached at a Bb concentration of 1-10 nM. Of note is the fact that antibody to Factor B recognized HMW-BCGF, and an mAb to HMW-BCGF also recognized Factor B and Bb, but not Ba. Moreover, radiolabeled Bb bound saturably to activated B cells and to an EBV-transformed human B cell line. The binding of Bb was inhibited by HMW-BCGF but not by Ba or IgG. Thus, Bb is antigenically and functionally related to HMW-BCGF, and can act as a B cell growth and differentiation factor at potentially physiologic concentrations. These data suggest that Bb may be important in amplifying the immune response in areas of inflammation. Since complement activation occurs at inflammatory sites long before induction of HMW-BCGF synthesis, Bb may be an early signal for the clonal expansion of antigen-activated B cells.

scholarly journals Antigen-independent regulation of cytoplasmic calcium in B cells with a 12-kDa B-cell growth factor and anti-CD19.

1988 ◽  
Vol 85 (6) ◽  
pp. 1897-1901 ◽  
Author(s):  
J. A. Ledbetter ◽  
P. S. Rabinovitch ◽  
C. H. June ◽  
C. W. Song ◽  
E. A. Clark ◽  
...  
Keyword(s):  
B Cells ◽  
Growth Factor ◽  
Cell Growth ◽  
B Cell ◽  
Cytoplasmic Calcium ◽  
B Cell Growth Factor

Membrane depolarization of human B cells follows stimulation by either anti-μ or B-cell growth factor, but only anti-μ causes cell volume changes

1988 ◽  
Vol 21 (3) ◽  
pp. 155-164
Author(s):  
Wayne M. Yokoyama ◽  
Millie M. Chien ◽  
Susan E. Engardt ◽  
Susan W. Aguiar ◽  
Robert F. Ashman
Keyword(s):  
B Cells ◽  
Growth Factor ◽  
Cell Growth ◽  
B Cell ◽  
Cell Volume ◽  
Membrane Depolarization ◽  
Volume Changes ◽  
Human B Cells ◽  
B Cell Growth Factor

scholarly journals Differential response of malignant human B-cells to anti-IgM immunoglobulin (anti-mu) and B-cell growth factor: unique direct cytotoxicity of anti-mu on prolymphocytic leukemia cells

Blood ◽  
1990 ◽  
Vol 76 (8) ◽  
pp. 1601-1606 ◽  
Author(s):  
CS Chan ◽  
F Soehnlen ◽  
GP Schechter
Keyword(s):  
B Cells ◽  
Growth Factor ◽  
Cell Growth ◽  
B Cell ◽  
Cell Cultures ◽  
Cell Subset ◽  
Thymidine Uptake ◽  
Prolymphocytic Leukemia ◽  
Direct Cytotoxicity ◽  
B Cell Growth Factor

Abstract We examined in vitro tritiated thymidine uptake by B cells from seven prolymphocytic leukemia (PLL), seven chronic lymphocytic leukemia (CLL), and four plasma cell leukemia (PCL) patients in response to culture with anti-human IgM antibody (anti-mu) and B-cell growth factor (BCGF). In contrast to the stimulatory effect observed in normal B-cell cultures, the divalent F(ab')2 anti-mu antibody uniquely inhibited the autonomous proliferation and induced marked cytotoxicity in six of seven PLL cell cultures independent of complement or Fc-receptor- mediated mechanisms. There was neither stimulation or inhibition of the slgM+ CLL or the slgM- PCL cells. The inhibitory effect on the PLL cells was observed at an anti-mu concentration below the stimulatory threshold for normal B cells. Significant impairment of trypan blue exclusion was delayed until 48 hours, with morphological cellular changes suggestive of a programmed cell death mechanism or apoptosis. The cytotoxicity was independent of the slgM-staining intensity or the autonomous and BCGF-augmented DNA synthetic activity of the PLL cells and was similar in patients with de novo PLL or with prolymphocytic transformation of CLL. Cells from a PLL patient were separated by elutriation into two fractions, a BCGF-unresponsive large “transformed” cell fraction with marked autonomous DNA synthesis and a smaller lymphoid cell subset with low 3H-thymidine uptake that could be augmented by BCGF. Both fractions were equally susceptible to the cytotoxic effect of anti-mu. These data suggest that certain slgM- bearing malignant B cells are susceptible to anti-mu-triggered cytotoxicity. They may represent the malignant counterpart of a “tolerogenic” normal B-cell subset, and the unique direct cytotoxicity of anti-mu may provide a therapeutic strategy specifically for PLL.

scholarly journals Purification to homogeneity of a high molecular weight human B cell growth factor; demonstration of specific binding to activated B cells; and development of a monoclonal antibody to the factor.

1985 ◽  
Vol 162 (4) ◽  
pp. 1319-1335 ◽  
Author(s):  
J L Ambrus ◽  
C H Jurgensen ◽  
E J Brown ◽  
A S Fauci
Keyword(s):  
Molecular Weight ◽  
Monoclonal Antibody ◽  
B Cells ◽  
Growth Factor ◽  
Cell Growth ◽  
B Cell ◽  
High Molecular Weight ◽  
Sodium Dodecyl ◽  
Western Blots ◽  
B Cell Growth Factor

High molecular weight B cell growth factor (HMW-BCGF) produced by a T cell line was purified to homogeneity and demonstrated to bind specifically to activated human B cells. A monoclonal antibody to HMW-BCGF was developed that (a) specifically inhibited the activity of HMW-BCGF in enhancing B cell proliferation, (b) specifically bound to HMW-BCGF in Western blots, (c) specifically absorbed HMW-BCGF activity from culture supernatants, and (d) specifically absorbed an internally labeled protein from T-ALL supernatant which comigrates with HMW-BCGF on sodium dodecyl sulfate-polyacrylamide gels. This antibody should help in cloning the gene for HMW-BCGF and further exploring the physiologic roles of HMW-BCGF.

Proliferation of B Cells from Chronic Lymphocytic Leukemia Is Selectively Promoted by B Cell Growth Factor

1989 ◽  
Vol 81 (2) ◽  
pp. 91-97 ◽  
Author(s):  
Melchor Alvarez-Mon ◽  
Antonio de la Hera ◽  
Maria Luisa Gaspar ◽  
Alberto Orfao ◽  
Juan Casas ◽  
...  
Keyword(s):  
B Cells ◽  
Growth Factor ◽  
Cell Growth ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Lymphocytic Leukemia ◽  
B Cell Growth Factor

scholarly journals Evidence for two distinct classes of murine B cell growth factors with activities in different functional assays.

1983 ◽  
Vol 158 (3) ◽  
pp. 822-835 ◽  
Author(s):  
S L Swain ◽  
M Howard ◽  
J Kappler ◽  
P Marrack ◽  
J Watson ◽  
...  
Keyword(s):  
Growth Factors ◽  
B Cells ◽  
Growth Factor ◽  
Cell Growth ◽  
B Cell ◽  
Functional Activity ◽  
Dextran Sulfate ◽  
Functional Assays ◽  
Cell Sources ◽  
B Cell Growth Factor

Several previously described B cell growth factor (BCGF) activities from a number of mouse monoclonal T cell sources were compared in different functional assays. The results indicate that there are two distinct classes of BCGF defined by functional activity and source. BCGF I, whose prototype is (EL4)BCGF, synergized with anti-Ig in the proliferation of normal splenic B cells but had no activity when dextran sulfate (DXS), rather than anti-Ig, was used to costimulate the same source of B cells. BCGF I also failed to directly stimulate BCL1 tumor B cells. In contrast, BCGF II, whose prototype is (DL)BCGF, showed a reciprocal pattern of activity. BCGF II failed to synergize with anti-Ig-costimulated normal B cells to give good proliferative responses. Sources of BCGF II also directly stimulated (no anti-Ig or DXS added) B cells of the BCL1 tumor-carrying mice. These results suggest that the two BCGF may have activity on two subsets of B cells that respond differentially to induction with the two polyclonal B cell activators, anti-Ig and DXS. The possibilities that these different patterns of response occur in separate lineages of B cells and/or in B cells in different states of differentiation is discussed.

scholarly journals Impaired responsiveness to B cell growth factor in a patient with common variable hypogammaglobulinemia

Blood ◽  
1985 ◽  
Vol 66 (2) ◽  
pp. 345-349 ◽  
Author(s):  
RT Perri ◽  
DJ Weisdorf
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
B Cells ◽  
Growth Factor ◽  
Cell Growth ◽  
B Cell ◽  
Immunoglobulin Synthesis ◽  
B Cell Growth Factor ◽  
Common Variable ◽  
Cell Defect

Abstract Common variable hypogammaglobulinemia (CVH) is a clinical syndrome that includes a diverse group of patients with heterogeneous defects resulting in impaired B cell proliferation and terminal differentiation into mature plasma cells capable of normal immunoglobulin synthesis and secretion. In this study, we report our identification of a previously undescribed intrinsic B cell defect in a patient with CVH. This patient's B cells showed a marked impairment in hemolytic plaque- forming cell (HePFC) formation compared with control B cells (15 v 80 HePFCs per culture, respectively). In addition, this patient's B cells displayed decreased B cell colony formation compared with control B cells (5 +/- 2 v 93 +/- 8, respectively). When examined for their responsiveness to phytohemagglutinin-T cell conditioned media (PHA- TCM), the patient's B cells displayed impaired B cell proliferation compared with control B cells (stimulation index [SI] 1.3 +/- 0.20 v 26 +/- 1.4 with 20% control PHA-TCM [vol/vol]). Impaired proliferation by the patient's B cells persisted with increasing concentrations of B cell growth factor (BCGF). Additionally, PHA-TCM prepared from the patient's T cells when compared with control PHA-TCM consistently showed less support for control B cell proliferation (SI 1.27 +/- 0.21 v 26 +/- 1.4, respectively). In coculture studies of B cell proliferation and immunoglobulin synthesis, patient's T cells showed no evidence of an enhanced suppressive effect or decreased helper effect. This patient's immune defects involve, first, an intrinsic B cell defect characterized by an impaired responsiveness to BCGF's proliferation signal and, second, impaired production of BCGF by the patient's T cells.

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