Normal and Neoplastic B Lymphocytes Produce Interleukin-1 (IL-1) and Colony Stimulating Factor (CSF)

Pistoia, Vito; Cozzolino, Federico; Ghio, Riccardo; Castigli, Emanuela; Torcia, M; Zupo, Simona; Rubartelli, Anna; Roncella, Silvio; Ferrarini, Manlio

doi:10.1007/978-1-4684-7035-2_21

Cited by 6 publications

(10 citation statements)

References 5 publications

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“…Megakaryocytic cell lines have also been reported to express several cytokine genes (29). In addition, both B cells (30)(31)(32) and NK cells (33)(34)(35) tAlso of note in this regard is the demonstration that PDGF stimulates the growth of primitive hematopoietic cells (pre-CFC multi) by inducing IL-1 production in a subset of macrophages (53).…”

Section: Discussionmentioning

confidence: 99%

Regulated production of a pleiotropic cytokine-platelet-derived growth factor--by differentiating erythroid cells in vitro and in vivo.

Keutzer

Sytkowski²

1995

Proc. Natl. Acad. Sci. U.S.A.

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Erythroid progenitor growth in vitro is stimulated by exogenous platelet-derived growth factor (PDGF). We now report that both normal and transformed erythroid progenitor cells produce authentic PDGF in vitro and in vivo. Importantly, this production is highly regulated during erythropoiesis. Addition of soluble lysates from Rauscher murine erythroleukemia cells-an erythropoietin-responsive model progenitor cell line-to quiescent BALB/c 3T3 fibroblasts resulted in a mitogenic response identical to that observed with the addition of authentic recombinant PDGF. Polyclonal and monoclonal anti-PDGF antibodies immunoabsorbed 50-100% of this activity. Induction of Rauscher cell differentiation in vitro with dimethyl sulfoxide or erythropoietin for 48-72 hr markedly upregulated PDGF production by 17-to 18-fold and 14-to 38-fold, respectively. Importantly, stimulation of normal erythropoiesis in vivo in mice treated either with phenylhydrazine or with erythropoietin increased PDGF levels in the spleen by 11-to 48-fold and 20-to 34-fold, respectively. These results strongly suggest a role for erythroid cell-derived PDGF in normal erythropoiesis and provide documentation of the regulated production of a pleiotropic cytokine by erythroid cells.The growth and differentiation of erythroid progenitors in vitro are enhanced markedly by the addition of platelet-derived growth factor (PDGF) (1,2). The mechanism through which PDGF exerts this effect is unknown. Stimulation of erythroid cells by PDGF may occur by direct activation of the progenitors themselves or may be mediated through another cell type via a so-called paracrine mechanism. Several types of cells, including some transformed cell lines with erythroid characteristics, produce PDGF-like activity or can be induced to do so (3, 4). In the case of the transformed erythroid cells, it had been speculated originally that the production of PDGF was consequential to their transformation rather than characteristic of their erythroid phenotype.Previously, we demonstrated that both erythropoietin (Epo)-responsive Rauscher murine erythroleukemia cells and the splenic erythroid cells of phenylhydrazine (PHZ)-treated mice produce a PDGF-like activity that stimulates erythropoiesis in vitro (5). We now show that these "PDGF-like molecules" are authentic PDGF. Moreover, our results demonstrate that the production of erythroid cell-derived PDGF is highly regulated during erythropoiesis in vivo and erythroid differentiation in vitro. MATERIALS AND METHODSCells. The continuous Rauscher murine erythroleukemia cell line (6, 7) (clone R404) and murine BALB/c 3T3 fibro-The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. Control splenocytes, the majority of which are B and T lymphocytes, were obtained from B6C3F1 mice. To induce splenic erythropoiesis, B6C3F1 mice were injected subcutaneously either with recombinant human Ep...

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Section: Discussionmentioning

confidence: 99%

Regulated production of a pleiotropic cytokine-platelet-derived growth factor--by differentiating erythroid cells in vitro and in vivo.

Keutzer

Sytkowski²

1995

Proc. Natl. Acad. Sci. U.S.A.

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“…The rosetting cells were removed from non-rosetting cells (B cells) on two consecutive FicollHypaque (F-H) density gradients [16]. B cells were separated into fractions of different density by discontinuous Percoll (Pharmacia) gradients.…”

Section: Cell Cultures 21 Cells and Cell Fractionation Proceduresmentioning

confidence: 99%

“…Purified B cells were obtained by rosetting tonsillar mononuclear cells (MNC) with neuraminidase-treated sheep erythrocytes [16]. The rosetting cells were removed from non-rosetting cells (B cells) on two consecutive FicollHypaque (F-H) density gradients [16].…”

Section: Cell Cultures 21 Cells and Cell Fractionation Proceduresmentioning

confidence: 99%

Expression of CD5 and CD38 by human CD5⁻ B cells: Requirement for special stimuli

Zupo¹,

Dono²,

Massara³

et al. 1994

Eur J Immunol

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In this study the mode of expression of CD5 by human tonsillar CD5- B cells after stimulation with different agents was investigated. Resting B cells were separated into CD5+ and CD5- cells and the two cell fractions exposed to phorbol 12-myristate 13-acetate (PMA). CD5- B cells expressed CD5 and maximum CD5 expression was achieved after approximately 60 h of culture. Based upon the proportions of cells that express CD5 as well as those of the cells surviving in culture, it was calculated that 15-25% of the total CD5- B cells were induced to express CD5. Unlike CD5- B cells, CD5+ B cells proliferated vigorously in response to PMA as assessed by [3H]thymidine incorporation and cell cycle analysis in vitro. However, the expression of CD5 by CD5- B cells was not related to the selective expansion of some CD5+ B cells left over as contaminant cells since this occurred in the absence of cell proliferation. Upon exposure to PMA, CD5- B cells remained in the G0-G1 phases of the cell cycle and did not express the Ki67 antigen or incorporate [3H]thymidine. Furthermore, mitomycin C treatment of the CD5- B cells did not prevent CD5 expression. Phenotypic studies disclosed that CD5+ B cells but not CD5- B cells expressed CD39. This finding offered the opportunity to carry out an additional control experiment. Separation of the two populations according to the expression of CD39 confirmed the finding obtained by fractionating the cells into CD5+ and CD5- B cells. The cells induced to express CD5 also expressed CD38 that was not detected on resting CD5- B cells. In this respect, the CD5- B cells that converted into CD5+ cells (inducible CD5+ B cells) resembled the cells from the CD5+ B cell fractions that up-regulated CD5 and also expressed CD38 upon exposure to PMA alone. Another example of coordinate expression of these two antigens was the finding that exposure to PMA in the presence of recombinant interleukin-4 (rIL-4) resulted in inhibition of the expression of CD5 and CD38. Although virtually all of the tonsillar CD5- B cells expressed the CD69 activation marker, no cells other than those co-expressing CD5 and CD38 were induced to express CD5 by PMA alone. Resting CD5- B cells failed to express CD5 and/or CD38 when cultured with PMA in the presence of EL4 T cells and IL-4-free T cell supernatants.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…The events that are influenced by IL-1 include synthesis of acute phase proteins by hepatocytes, release of degradative enzymes from connective tissue cells, and proliferation of lymphocytes (1). Among the leukocytes, macrophages, lymphocytes, and dendritic cells have all been implicated in production of IL-1 (2)(3)(4)(5)(6)(7)(8).…”

mentioning

confidence: 99%

Induction of murine interleukin 1: stimuli and responsive primary cells.

Koide¹,

Steinman²

1987

Proc. Natl. Acad. Sci. U.S.A.

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An interleukin 1a (IL-1a) cDNA probe and an IL-l responsive T-cell clone (D1O.G4; half-maximal stimulation, 0.1-1 pM) have been used to study the production of IL-1 by primary murine cell populations, particularly macrophages and dendritic cells. Spleen and peritoneal macrophages produced IL-1 mRNA and released biologically active IL-1 when challenged with lipopolysaccharide (LPS). Induction of IL-1 was evident over a dose range of 0.01-10 ,jg of LPS per ml, and maxmal mRNA levels were maintained from 4 to 20 hr. Several other stimuli did not induce IL-1 in cultured macrophages, including phorbol 12-myristate 13-acetate, r-interferon, Con A, macrophage colony-stimulating factor, IL-3, cachectin, and activated T cells. Activated T cells could markedly reduce the response ofperitoneal macrophages to LPS. When other cell types were compared with macrophages, keratinocytes had high levels of IL-1 mRNA, apparently in response to endogenous LPS. However B and T lymphocytes did not yield detectable IL-1 during proliferative responses to LPS and Con A, respectively, While dendritic cells produced little or no IL-1 when challenged with a battery of stimuli. Therefore, IL-1 may not be required for the potent accessory function of dendritic cells in lymphocyte mitogenesis. The results indicate that macrophages and dendritic cells have different secretory capacities. The macrophage is the principal leukocyte that synthesizes IL-1, and select stimuli increase and decrease the levels of macrophage IL-1 mRNA.

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Normal and Neoplastic B Lymphocytes Produce Interleukin-1 (IL-1) and Colony Stimulating Factor (CSF)

Cited by 6 publications

References 5 publications

Regulated production of a pleiotropic cytokine-platelet-derived growth factor--by differentiating erythroid cells in vitro and in vivo.

Regulated production of a pleiotropic cytokine-platelet-derived growth factor--by differentiating erythroid cells in vitro and in vivo.

Expression of CD5 and CD38 by human CD5⁻ B cells: Requirement for special stimuli

Induction of murine interleukin 1: stimuli and responsive primary cells.

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Normal and Neoplastic B Lymphocytes Produce Interleukin-1 (IL-1) and Colony Stimulating Factor (CSF)

Cited by 6 publications

References 5 publications

Regulated production of a pleiotropic cytokine-platelet-derived growth factor--by differentiating erythroid cells in vitro and in vivo.

Regulated production of a pleiotropic cytokine-platelet-derived growth factor--by differentiating erythroid cells in vitro and in vivo.

Expression of CD5 and CD38 by human CD5− B cells: Requirement for special stimuli

Induction of murine interleukin 1: stimuli and responsive primary cells.

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Expression of CD5 and CD38 by human CD5⁻ B cells: Requirement for special stimuli