Interleukin-4 induces secretion of CSF for granulocytes and CSF for macrophages by peripheral blood monocytes

Wieser, M.; Bonifer, R; Oster, W; Lindemann, A.; Mertelsmann, R; Herrmann, F

doi:10.1182/blood.v73.5.1105.bloodjournal7351105

Cited by 9 publications

(12 citation statements)

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“…Thus, the members oi the IFN-x//i gene family can be added to the other monocyte-derived cytokines, the production of which can be down-regulated by IL-4. Because M-CSF and G-CSF are actually induced in monocytes by IL-4 [16], the IL-4 has a differential action on cytokine responses in monocyles.…”

Section: Discussionmentioning

confidence: 99%

“…Several efFector functions are also stimulated by IL-4, including cytotoxicity against tumour cells [13,14], phagocytosis and inactivation of parasites [15]. as well as produelion of the eytokines M-CSF and G-CSF [16] and of tissue plasminogen activator [17]. The lL-4 also in-creases expression of class I and class II major histocompatibility complex antigens [12,13].…”

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confidence: 99%

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Interleukin‐4 Down‐Regulates Sendai Virus‐Induced Production of Interferon‐α and ‐β in Human Peripheral Blood Monocytes In Vitro

Gobl

Alm

1992

Scand J Immunol

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Recombinant interleukin-4 (rIL-4) caused a 65-70% reduction of the interferon-alpha (IFN-alpha) and -beta production induced by Sendai virus (SV) in human peripheral blood monocytes in vitro. Significant inhibition was seen at concentrations as low as 0.1 ng/ml. The rIL-4 also reduced levels of IFN-alpha and -beta mRNA by 60% and 67%, respectively, as well as the frequency of IFN-alpha and -beta mRNA-containing cells by 65% and 54%, respectively. The frequency of IFN-alpha/beta mRNA-containing cells was inhibited by rIL-4 throughout the whole course of induction by SV. IL-4 caused a shift of the grain count distribution towards less heavily labelled cells, suggesting an inhibitory effect of rIL-4 on most IFN-alpha/beta mRNA-containing cells. Antibodies to rIL-4 did not influence the normal IFN-alpha/beta response induced by SV, but abolished the inhibitory effect of the rIL-4. When rIL-4 was added to cells 4 h after start of stimulation by SV, at which time much mRNA has accumulated but little IFN-alpha/beta has been secreted, no inhibition of the IFN-alpha/beta production by rIL-4 was seen. IFN-gamma had only a minor reversing effect on the rIL-4 inhibition, but if cells were precultivated in medium with or without IFN-gamma for 6 h before SV induction, rIL-4 paradoxically enhanced the IFN-alpha/beta response. Our results suggest that rIL-4 inhibits an early step of IFN-alpha/beta induction in monocytes, at the level either of transcription of IFN-alpha/beta genes or of the processing or stability of mRNA. The IL-4 effects may however depend on the state of activation of the monocytes.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Interleukin‐4 Down‐Regulates Sendai Virus‐Induced Production of Interferon‐α and ‐β in Human Peripheral Blood Monocytes In Vitro

Gobl

Alm

1992

Scand J Immunol

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“…In contrast, other investigators have demonstrated that hIL-4 suppresses IL-3-dependent erythroid burst formation from normal human BM, but enhances the proliferation of normal peripheral blood (PB)-derived BFU-E (De Wolf et al, 1990. These discrepancies may be explained by differences in the target populations as well as the presence or absence of accessory cells in cultures, since IL-4 can act on cells directly and indirectly (Broxmeyer et al, 1988;Wisser et al, 1989).…”

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confidence: 99%

Action of human interleukin‐4 and stem cell factor on erythroid and mixed colony formation by peripheral blood‐derived CD34⁺c‐kit^high or CD34⁺c‐kit^low cells

Sonoda¹,

Kimura²,

Ohmizono³

et al. 1997

Br J Haematol

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We studied the interaction of interleukin (IL)‐4 and other burst‐promoting activity (BPA) factors, such as IL‐3, granulocyte/macrophage colony‐stimulating factor (GM‐CSF), IL‐9 and stem cell factor (SCF), on erythroid burst‐forming unit (BFU‐E) and erythrocyte‐containing mixed (CFU‐Mix) colony formation in serum‐free culture. IL‐4 alone did not support mixed colony formation in the presence of erythropoietin (Epo). However, IL‐4 showed weak but significant BPA when peripheral blood (PB)‐derived CD34+c‐kitlow cells were used as the target population. The BPA of IL‐4 was much weaker than that of IL‐3, which exerted the most potent activity, as previously reported. When CD34+c‐kithigh cells were used as the target, four factors known to have BPA, IL‐3, GM‐CSF, IL‐9 and SCF, could express BPA. In contrast, IL‐4 alone failed to support erythroid burst formation. Interestingly, IL‐4 showed a remarkable enhancing effect with SCF in promoting the development of erythroid burst and erythrocyte‐containing mixed colonies from CD34+c‐kitlow and CD34+c‐kithigh cells. Delayed addition of SCF + Epo or IL‐4+Epo to the cultures initiated with either IL‐4 or SCF alone clearly demonstrated that SCF was a survival factor for both BFU‐E and CFU‐Mix progenitors. In contrast, the survival effect of IL‐4 was much weaker than that of SCF, and appeared to be more important for progenitors derived from CD34+c‐kitlow cells than for those derived from CD34+c‐kithigh cells. It was recently reported that CD34+c‐kitlow cells represent a more primitive population than CD34+c‐kithigh cells. Taken together, these results suggest that IL‐4 helps to recruit primitive progenitor cells in the presence of SCF.

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“…11,12 On the other hand, IL-4 stimulates the production of G-and M-CSF. 13 Depending on: (i) the differentiation state of monocytes/macrophages, and (ii) the activation signal provided (lipopolysaccharide or IFN-g), IL-4 differentially reg-ulates the generation of oxygen derivatives, H 2 O 2 , O 2 14-16 and nitric oxide. [17][18][19] Recent observations from our laboratory indicated that LTB 4 , a 5-lipoxygenase metabolite that is produced by macrophages during inflammatory reactions, enhanced some of the biological effects of IL-4, namely CD23 expression and its release by human monocytes and B lymphocytes 20,21 and IgE production by normal human peripheral blood mononuclear cells 22 possibly by interfering with the signalling pathway of IL-4 in target cells.…”

Section: Introductionmentioning

confidence: 99%

Role of leukotriene B₄ in the interleukin‐4‐induced human mononuclear phagocyte activation

Dugas¹,

Dugas²,

Kolb

et al. 1996

Immunology

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SUMMARYInterleukin-4 (IL-4) induced a time-and dose-dependent production of leukotriene B 4 (LTB 4 ) by human resting monocytes indicating that IL-4 induced the activation of the 5-lipoxygenase pathway in resting human monocytes. Maximal effect was observed in the presence of 10 ng/ml IL-4, and in kinetics experiments LTB 4 production plateaued 40 min after the onset of stimulation. When stimulated for 48 hr with IL-4, resting human monocytes expressed and released the low-affinity receptor for IgE (CD23) and were partially inhibited in the presence of a highly non-redox 5-lipoxygenase inhibitor (BW B70C), suggesting that the production of LTB 4 partially contributed to the IL-4-induced CD23 expression and release. This hypothesis was strengthened by the fact that exogenous LTB 4 (10 nM) was found to increase the effect of a suboptimal dose of IL-4 (1 ng/ml). In addition to these phenotypical changes, IL-4 primed the phorbol-12-myristate-13-acetate (PMA)-induced luminol-dependent chemiluminescence response (LDCL) by normal human monocytes, this priming effect being abrogated in the presence of BW B70C. Taken together, these data indicated that IL-4 induced the production of LTB 4 by activation of the 5-lipoxygenase pathway in human monocytes, and that the activation of this pathway could upregulate the expression and release of CD23 and the respiratory burst of these cells.

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Interleukin-4 induces secretion of CSF for granulocytes and CSF for macrophages by peripheral blood monocytes

Cited by 9 publications

References 0 publications

Interleukin‐4 Down‐Regulates Sendai Virus‐Induced Production of Interferon‐α and ‐β in Human Peripheral Blood Monocytes In Vitro

Interleukin‐4 Down‐Regulates Sendai Virus‐Induced Production of Interferon‐α and ‐β in Human Peripheral Blood Monocytes In Vitro

Action of human interleukin‐4 and stem cell factor on erythroid and mixed colony formation by peripheral blood‐derived CD34⁺c‐kit^high or CD34⁺c‐kit^low cells

Role of leukotriene B₄ in the interleukin‐4‐induced human mononuclear phagocyte activation

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Interleukin-4 induces secretion of CSF for granulocytes and CSF for macrophages by peripheral blood monocytes

Cited by 9 publications

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Interleukin‐4 Down‐Regulates Sendai Virus‐Induced Production of Interferon‐α and ‐β in Human Peripheral Blood Monocytes In Vitro

Interleukin‐4 Down‐Regulates Sendai Virus‐Induced Production of Interferon‐α and ‐β in Human Peripheral Blood Monocytes In Vitro

Action of human interleukin‐4 and stem cell factor on erythroid and mixed colony formation by peripheral blood‐derived CD34+c‐kithigh or CD34+c‐kitlow cells

Role of leukotriene B4 in the interleukin‐4‐induced human mononuclear phagocyte activation

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Action of human interleukin‐4 and stem cell factor on erythroid and mixed colony formation by peripheral blood‐derived CD34⁺c‐kit^high or CD34⁺c‐kit^low cells

Role of leukotriene B₄ in the interleukin‐4‐induced human mononuclear phagocyte activation