B-cell-derived granulocyte-colony stimulating factor (G-CSF)

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Biologically active granulocyte-colony stimulating factor (G-CSF) was released spontaneously in culture by in vivo activated tonsillar B lymphocytes and, in particular, by the germinal center (GC) B-cell subset. In contrast, mantle zone B cells failed to produce the cytokine under any of the culture conditions tested. A CD40 monoclonal antibody (mAb), recombinant (r) IL4, and the combination of the CD40 mAb and rIL4 all increased G-CSF production by GC B cells. The augmentation of G-CSF release correlated with the increased survival of GC B cells. rG-CSF rescued GC B cells from apoptosis, suggesting that the cytokine may be utilized in autocrine and/or paracrine ways. Neoplastic B cells from follicular center cell lymphoma patients, which are the counterparts of normal GC B lymphocytes, also released G-CSF spontaneously in culture. In contrast, malignant B cells from a subset of chronic lymphocytic leukemia (CLL) patients had to be stimulated with Staphylococcus aureus Cowan I or CD40 mAb in combination with rIL4 or rIL2 to produce G-CSF in vitro. Some B-CLL cell suspensions were rescued from spontaneous apoptosis following culture in the presence of rG-CSF. Taken together, these studies provide the first demonstration that GCSF (i) is produced by either normal or neoplastic human B lymphocytes and (ii) participates in the modulation of apoptosis of the same cells.

Original languageEnglish
Pages (from-to)143-147
Number of pages5
JournalMethods in Enzymology
Volume11
Issue number1
DOIs
Publication statusPublished - Jan 1997

Fingerprint

Granulocyte Colony-Stimulating Factor
B-Lymphocytes
Germinal Center
Cells
Lymphocytes
B-Lymphocyte Subsets
Monoclonal Antibodies
Apoptosis
Cell culture
B-Cell Chronic Lymphocytic Leukemia
Cytokines
Interleukin-4
Suspensions
Demonstrations
Staphylococcus aureus
Lymphoma
Modulation

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Molecular Biology

Cite this

B-cell-derived granulocyte-colony stimulating factor (G-CSF). / Corcione, Anna; Pistoia, Vito.

In: Methods in Enzymology, Vol. 11, No. 1, 01.1997, p. 143-147.

Research output: Contribution to journalArticle

@article{63697c3f1c9340cbbd218cbbcbed77f3,
title = "B-cell-derived granulocyte-colony stimulating factor (G-CSF)",
abstract = "Biologically active granulocyte-colony stimulating factor (G-CSF) was released spontaneously in culture by in vivo activated tonsillar B lymphocytes and, in particular, by the germinal center (GC) B-cell subset. In contrast, mantle zone B cells failed to produce the cytokine under any of the culture conditions tested. A CD40 monoclonal antibody (mAb), recombinant (r) IL4, and the combination of the CD40 mAb and rIL4 all increased G-CSF production by GC B cells. The augmentation of G-CSF release correlated with the increased survival of GC B cells. rG-CSF rescued GC B cells from apoptosis, suggesting that the cytokine may be utilized in autocrine and/or paracrine ways. Neoplastic B cells from follicular center cell lymphoma patients, which are the counterparts of normal GC B lymphocytes, also released G-CSF spontaneously in culture. In contrast, malignant B cells from a subset of chronic lymphocytic leukemia (CLL) patients had to be stimulated with Staphylococcus aureus Cowan I or CD40 mAb in combination with rIL4 or rIL2 to produce G-CSF in vitro. Some B-CLL cell suspensions were rescued from spontaneous apoptosis following culture in the presence of rG-CSF. Taken together, these studies provide the first demonstration that GCSF (i) is produced by either normal or neoplastic human B lymphocytes and (ii) participates in the modulation of apoptosis of the same cells.",
author = "Anna Corcione and Vito Pistoia",
year = "1997",
month = "1",
doi = "10.1006/meth.1996.0398",
language = "English",
volume = "11",
pages = "143--147",
journal = "ImmunoMethods",
issn = "1046-2023",
publisher = "Academic Press Inc.",
number = "1",

}

TY - JOUR

T1 - B-cell-derived granulocyte-colony stimulating factor (G-CSF)

AU - Corcione, Anna

AU - Pistoia, Vito

PY - 1997/1

Y1 - 1997/1

N2 - Biologically active granulocyte-colony stimulating factor (G-CSF) was released spontaneously in culture by in vivo activated tonsillar B lymphocytes and, in particular, by the germinal center (GC) B-cell subset. In contrast, mantle zone B cells failed to produce the cytokine under any of the culture conditions tested. A CD40 monoclonal antibody (mAb), recombinant (r) IL4, and the combination of the CD40 mAb and rIL4 all increased G-CSF production by GC B cells. The augmentation of G-CSF release correlated with the increased survival of GC B cells. rG-CSF rescued GC B cells from apoptosis, suggesting that the cytokine may be utilized in autocrine and/or paracrine ways. Neoplastic B cells from follicular center cell lymphoma patients, which are the counterparts of normal GC B lymphocytes, also released G-CSF spontaneously in culture. In contrast, malignant B cells from a subset of chronic lymphocytic leukemia (CLL) patients had to be stimulated with Staphylococcus aureus Cowan I or CD40 mAb in combination with rIL4 or rIL2 to produce G-CSF in vitro. Some B-CLL cell suspensions were rescued from spontaneous apoptosis following culture in the presence of rG-CSF. Taken together, these studies provide the first demonstration that GCSF (i) is produced by either normal or neoplastic human B lymphocytes and (ii) participates in the modulation of apoptosis of the same cells.

AB - Biologically active granulocyte-colony stimulating factor (G-CSF) was released spontaneously in culture by in vivo activated tonsillar B lymphocytes and, in particular, by the germinal center (GC) B-cell subset. In contrast, mantle zone B cells failed to produce the cytokine under any of the culture conditions tested. A CD40 monoclonal antibody (mAb), recombinant (r) IL4, and the combination of the CD40 mAb and rIL4 all increased G-CSF production by GC B cells. The augmentation of G-CSF release correlated with the increased survival of GC B cells. rG-CSF rescued GC B cells from apoptosis, suggesting that the cytokine may be utilized in autocrine and/or paracrine ways. Neoplastic B cells from follicular center cell lymphoma patients, which are the counterparts of normal GC B lymphocytes, also released G-CSF spontaneously in culture. In contrast, malignant B cells from a subset of chronic lymphocytic leukemia (CLL) patients had to be stimulated with Staphylococcus aureus Cowan I or CD40 mAb in combination with rIL4 or rIL2 to produce G-CSF in vitro. Some B-CLL cell suspensions were rescued from spontaneous apoptosis following culture in the presence of rG-CSF. Taken together, these studies provide the first demonstration that GCSF (i) is produced by either normal or neoplastic human B lymphocytes and (ii) participates in the modulation of apoptosis of the same cells.

UR - http://www.scopus.com/inward/record.url?scp=0030950002&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030950002&partnerID=8YFLogxK

U2 - 10.1006/meth.1996.0398

DO - 10.1006/meth.1996.0398

M3 - Article

C2 - 8990100

AN - SCOPUS:0030950002

VL - 11

SP - 143

EP - 147

JO - ImmunoMethods

JF - ImmunoMethods

SN - 1046-2023

IS - 1

ER -