scholarly journals Requirement for Rictor in homeostasis and function of mature B lymphoid cells

Blood ◽  
2013 ◽  
Vol 122 (14) ◽  
pp. 2369-2379 ◽  
Author(s):  
Keunwook Lee ◽  
Lindsey Heffington ◽  
Julia Jellusova ◽  
Ki Taek Nam ◽  
Ariel Raybuck ◽  
...  
Keyword(s):  
Gene Expression ◽  
B Cells ◽  
Lymphoid Cells ◽  
Key Points ◽  
Antiapoptotic Gene ◽  
B Lymphoid ◽  
And Function

Key Points Maturation, homeostasis, and function of peripheral B lymphoid cells require Rictor, an essential mTOR complex 2 component. Rictor regulates survival of B cells and their balance of proapoptotic vs antiapoptotic gene expression.

scholarly journals Mitogen plus interleukin 4 induction of C epsilon transcripts in B lymphoid cells.

1988 ◽  
Vol 168 (6) ◽  
pp. 2385-2389 ◽  
Author(s):  
P Rothman ◽  
S Lutzker ◽  
W Cook ◽  
R Coffman ◽  
F W Alt
Keyword(s):  
B Cells ◽  
Differential Expression ◽  
Lymphoid Cells ◽  
Interleukin 4 ◽  
Transformed Cells ◽  
Rna Expression ◽  
Concomitant Treatment ◽  
Constant Region ◽  
Induced Expression ◽  
B Lymphoid

To elucidate the mechanism of IL-4-induced enhancement of IgE and IgG1 production, murine splenic B cells and A-MuLV-transformed cells were cultured with LPS and IL-4 and assayed for epsilon and gamma 1 transcripts. Concomitant treatment with IL-4 and LPS induced expression of C epsilon transcripts in both normal and transformed cells. Expression of these truncated C epsilon transcripts preceded accumulation of normal epsilon mRNA in treated cells. Consistent data were obtained with respect to gamma 1 RNA expression. These results suggest that IL-4 can direct class switching in the context of a mechanism associated with differential expression of germline constant region genes.

scholarly journals xB elements strongly activate gene expression in non-lymphoid cells and function synergistically with NF1 elements

1989 ◽  
Vol 17 (20) ◽  
pp. 8197-8206 ◽  
Author(s):  
Lothar Henninghausen ◽  
Priscilla A. Furth ◽  
Chirstoph W. Pittius
Keyword(s):  
Gene Expression ◽  
Lymphoid Cells ◽  
And Function ◽  
Activate Gene

scholarly journals Oncogene cooperation in lymphocyte transformation: malignant conversion of E mu-myc transgenic pre-B cells in vitro is enhanced by v-H-ras or v-raf but not v-abl.

1989 ◽  
Vol 9 (1) ◽  
pp. 67-73 ◽  
Author(s):  
W S Alexander ◽  
J M Adams ◽  
S Cory
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Bone Marrow Cells ◽  
Lymphocyte Transformation ◽  
Lymphoid Cells ◽  
B Lineage ◽  
B Lymphoid ◽  
Marrow Cells ◽  
B Lineage Cells

Although transgenic mice bearing a c-myc gene controlled by the immunoglobulin heavy-chain enhancer (E mu) eventually develop B-lymphoid tumors, B-lineage cells from preneoplastic bone marrow express the transgene but do not grow autonomously or produce tumors in mice. To determine whether other oncogenes can cooperate with myc to transform B-lineage cells, we compared the in vitro growth and tumorigenicity of normal and E mu-myc bone marrow cells infected with retroviruses bearing the v-H-ras, v-raf, or v-abl oncogene. The v-H-ras and v-raf viruses both generated a rapid polyclonal expansion of E mu-myc pre-B bone marrow cells in liquid culture and 10- to 100-fold more pre-B lymphoid colonies than normal in soft agar. The infected transgenic cells were autonomous, cloned efficiently in agar, and grew as tumors in nude mice. While many pre-B cells from normal marrow could also be induced to proliferate by the v-raf virus, these cells required a stromal feeder layer, did not clone in agar, and were not malignant. Most normal cells stimulated to grow by v-H-ras also cloned poorly in agar, and only rare cells were tumorigenic. With the v-abl virus, no more cells were transformed from E mu-myc than normal marrow and the proportion of tumorigenic pre-B clones was not elevated. These results suggest that both v-H-ras and v-raf, but apparently not v-abl, collaborate with constitutive myc expression to promote autonomous proliferation and tumorigenicity of pre-B lymphoid cells.

scholarly journals Differential gene expression in chicken primary B cells infected ex vivo with attenuated and very virulent strains of infectious bursal disease virus (IBDV)

2017 ◽  
Author(s):  
Katherine L. Dulwich ◽  
Efstathios S. Giotis ◽  
Alice Gray ◽  
Venugopal Nair ◽  
Michael A. Skinner ◽  
...  
Keyword(s):  
Gene Expression ◽  
B Cells ◽  
B Cell ◽  
Disease Virus ◽  
Infectious Bursal Disease Virus ◽  
Ex Vivo ◽  
Lymphoid Cells ◽  
Infectious Bursal Disease ◽  
Type I ◽  
Bursal Disease

AbstractInfectious bursal disease virus (IBDV) belongs to the family Birnaviridae and is economically important to the poultry industry worldwide. IBDV infects B cells in the bursa of Fabricius (BF), causing immunosuppression and morbidity in young chickens. In addition to strains that cause classical Gumboro disease, the so-called ‘very virulent’ (vv) strain, also in circulation, causes more severe disease and increased mortality. IBDV has traditionally been controlled through the use of live attenuated vaccines, with attenuation resulting from serial passage in non-lymphoid cells. However, the factors that contribute to the vv or attenuated phenotypes are poorly understood. In order to address this, we aimed to investigate host cell-IBDV interactions using a recently described chicken primary B cell model, where chicken B cells are harvested from the BF and cultured ex vivo in the presence of chicken CD40L. We demonstrated that these cells could support the replication of IBDV when infected ex vivo in the laboratory. Furthermore, we evaluated the gene expression profiles of B cells infected with an attenuated strain (D78) and a very virulent strain (UK661) by microarray. We found that key genes involved in B cell activation and signaling (TNFSF13B, CD72 and GRAP) were down-regulated following infection relative to mock, which we speculate could contribute to IBDV-mediated immunosuppression. Moreover, cells responded to infection by expressing antiviral type I IFNs and IFN-stimulated genes, but the induction was far less pronounced upon infection with UK661, which we speculate could contribute to its virulence.

Oncogene cooperation in lymphocyte transformation: malignant conversion of E mu-myc transgenic pre-B cells in vitro is enhanced by v-H-ras or v-raf but not v-abl

1989 ◽  
Vol 9 (1) ◽  
pp. 67-73
Author(s):  
W S Alexander ◽  
J M Adams ◽  
S Cory
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Bone Marrow Cells ◽  
Lymphocyte Transformation ◽  
Lymphoid Cells ◽  
B Lineage ◽  
B Lymphoid ◽  
Marrow Cells ◽  
B Lineage Cells

Although transgenic mice bearing a c-myc gene controlled by the immunoglobulin heavy-chain enhancer (E mu) eventually develop B-lymphoid tumors, B-lineage cells from preneoplastic bone marrow express the transgene but do not grow autonomously or produce tumors in mice. To determine whether other oncogenes can cooperate with myc to transform B-lineage cells, we compared the in vitro growth and tumorigenicity of normal and E mu-myc bone marrow cells infected with retroviruses bearing the v-H-ras, v-raf, or v-abl oncogene. The v-H-ras and v-raf viruses both generated a rapid polyclonal expansion of E mu-myc pre-B bone marrow cells in liquid culture and 10- to 100-fold more pre-B lymphoid colonies than normal in soft agar. The infected transgenic cells were autonomous, cloned efficiently in agar, and grew as tumors in nude mice. While many pre-B cells from normal marrow could also be induced to proliferate by the v-raf virus, these cells required a stromal feeder layer, did not clone in agar, and were not malignant. Most normal cells stimulated to grow by v-H-ras also cloned poorly in agar, and only rare cells were tumorigenic. With the v-abl virus, no more cells were transformed from E mu-myc than normal marrow and the proportion of tumorigenic pre-B clones was not elevated. These results suggest that both v-H-ras and v-raf, but apparently not v-abl, collaborate with constitutive myc expression to promote autonomous proliferation and tumorigenicity of pre-B lymphoid cells.

Perturbation of B-cell development in mice overexpressing the Bcl-2 homolog A1

Blood ◽  
2002 ◽  
Vol 99 (9) ◽  
pp. 3350-3359 ◽  
Author(s):  
Peter I. Chuang ◽  
Samantha Morefield ◽  
Chien-Ying Liu ◽  
Stephen Chen ◽  
John M. Harlan ◽  
...  
Keyword(s):  
Immune System ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
System Development ◽  
Cell Development ◽  
B Cell Development ◽  
Lymphoid Cells ◽  
Immune System Development ◽  
And Function

Abstract Decisions about cell survival or death are central components of adaptive immunity and occur at several levels in immune system development and function. The Bcl-2 family of homologous proteins plays an important role in these decisions in lymphoid cells. Bcl-2, Bcl-xL, and A1 are differentially expressed during B- and T-cell development, and they have shared and distinct roles in regulating cell death. We sought to gain insight into the role of A1 in immune system development and function. A murine A1-a transgene was expressed under the control of the Eμ enhancer, and mice with A1 overexpression in B- and T-cell lineages were derived. Thymocytes and early B cells in Eμ-A1 mice showed extended survival. B-lineage development was altered, with expansion of the pro–B cell subset at the expense of pre–B cells, suggesting an impairment of the pro– to pre–B-cell transition. This early B-cell phenotype resembled Eμ–Bcl-xL mice but did not preferentially rescue cells with completed V(D)J rearrangements of the immunoglobulin heavy chain. In contrast to Eμ–Bcl-2 transgenes, A1 expression in pro–B cells did not rescue pre–B-cell development in SCID mice. These studies indicate that A1 protects lymphocytes from apoptosis in vitro but that it has lineage- and stage-specific effects on lymphoid development. Comparison with the effects of Bcl-2 and Bcl-xL expressed under similar control elements supports the model that antiapoptotic Bcl-2 homologs interact differentially with intracellular pathways affecting development and apoptosis in lymphoid cells.

scholarly journals Progenitor B-1 B-cell acute lymphoblastic leukemia is associated with collaborative mutations in 3 critical pathways

2017 ◽  
Vol 1 (20) ◽  
pp. 1749-1759 ◽  
Author(s):  
Sheryl M. Gough ◽  
Liat Goldberg ◽  
Marbin Pineda ◽  
Robert L. Walker ◽  
Yuelin J. Zhu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Lymphoblastic Leukemia ◽  
B Cells ◽  
B Cell ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Lymphoblastic Leukemia ◽  
Critical Pathways ◽  
Key Points ◽  
Cell Acute Lymphoblastic Leukemia

Key Points An NUP98-PHF23 fusion collaborates with acquired Bcor and Jak/Stat mutations to produce a pro–B-1 ALL. Gene expression profile of murine pro–B-1 ALL resembles that of a subset of human ALL, suggesting some human ALLs arise from pro–B-1 B cells.

scholarly journals Glucose metabolism impacts the spatiotemporal onset and magnitude of HSC induction in vivo

Blood ◽  
2013 ◽  
Vol 121 (13) ◽  
pp. 2483-2493 ◽  
Author(s):  
James M. Harris ◽  
Virginie Esain ◽  
Gregory M. Frechette ◽  
Lauren J. Harris ◽  
Andrew G. Cox ◽  
...  
Keyword(s):  
Gene Expression ◽  
Glucose Metabolism ◽  
Cell Formation ◽  
Oxygen Species ◽  
Hematopoietic Stem ◽  
Key Points ◽  
Vertebrate Embryo ◽  
And Function ◽  
Relevant Gene

Key Points Glucose metabolism enhances hematopoietic stem cell formation and function in the vertebrate embryo Glucose metabolism modulates hif1α activity via mitochondrial generation of reactive oxygen species to impact HSC-relevant gene expression

scholarly journals Regulated expression and function of CD122 (interleukin-2/interleukin- 15R-beta) during lymphoid development

Blood ◽  
1996 ◽  
Vol 87 (1) ◽  
pp. 190-201 ◽  
Author(s):  
T Reya ◽  
JA Yang-Snyder ◽  
EV Rothenberg ◽  
SR Carding
Keyword(s):  
B Cells ◽  
Fetal Liver ◽  
Interleukin 2 ◽  
Lymphoid Cells ◽  
Lymphocyte Development ◽  
Hematopoietic Stem ◽  
Embryo Sections ◽  
And Function ◽  
Receptor Beta

To determine whether signaling via CD122 (interleukin-2 [IL-2]/IL-15 receptor beta-chain) plays a role in regulating the expansion and differentiation of lymphocyte precursors, we have characterized its expression and evaluated its ability to influence the activity of developing lymphoid cells. A significant fraction of Sca1+Lin- hematopoietic stem cells in day 12 fetal liver were found to be CD122+. CD122-mRNA+ and IL-2-mRNA+ cells were also localized in embryo sections within pharyngeal blood vessels adjacent to and surrounding the thymic analgen. This distribution is consistent with the migration of CD122+ progenitor cells from the liver to the developing thymus where a majority of Sca1+ intrathymic T-cell progenitors were CD122+. Analysis of CD122 expression in the day 12 fetal liver revealed that the majority of B220+ cells were CD122+. Furthermore, CD122 expression was restricted to the earliest B220+ cells (CD43+CD24-; prepro B cells; fraction A) that proliferate vigorously to IL-2 in the absence of any stromal cells, but not to IL-15. Consistent with a role for the IL-2/IL- 2R pathway in lymphocyte development is the progressive loss of B cells seen in IL-2-deficient mice. Together, these observations suggest that CD122 plays a role in regulating normal lymphocyte development in vivo.

scholarly journals Chloroquine affects biosynthesis of Ia molecules by inhibiting dissociation of invariant (gamma) chains from alpha-beta dimers in B cells.

1985 ◽  
Vol 162 (4) ◽  
pp. 1371-1376 ◽  
Author(s):  
J Nowell ◽  
V Quaranta
Keyword(s):  
B Cells ◽  
Antigen Processing ◽  
Surface Expression ◽  
Lymphoid Cells ◽  
Gamma Chain ◽  
Accessory Cells ◽  
Intracellular Compartments ◽  
Acidic Compartment ◽  
Alpha Beta ◽  
B Lymphoid

Biosynthetic conversion of Ia oligomers from three chains (alpha, beta, gamma) to two (alpha, beta) before surface expression was inhibited in B lymphoid cells by treatment with chloroquine, resulting in the accumulation of Ia complexes composed of mature alpha and beta chains, and gamma chains at various states of sialylation. Other stages of Ia biosynthesis and processing appeared unaffected, indicating that chloroquine selectively interfered with the gamma chain dissociating mechanism itself. Similar effects were also observed with ammonium chloride. Because of the nature of such lysosomotropic agents, these results suggest that an intracellular acidic compartment may be involved in processing Ia oligomers to accomplish dissociation from gamma chains. Since chloroquine is known to inhibit Ia-restricted antigen presentation in accessory cells, our results raise the possibility that the pathways of antigen processing and Ia biosynthesis may use some common intracellular compartments.

Sign in / Sign up

Export Citation Format

Share Document