Human peripheral blood basophils primed by interleukin 3 (IL-3) produce IL-4 in response to immunoglobulin E receptor stimulation.

Brunner, Thomas; Heusser, Christoph; Dahinden, Clemens A.

doi:10.1084/jem.177.3.605

Cited by 361 publications

(197 citation statements)

References 33 publications

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“…Inhibition studies using actinomycin D indicated that both the up-and the down-regulation of cytokine expression by IL-4 is regulated at the transcriptional level. Because we did not find any IL-4 production by mast cells themselves, IL-4 that may regulate cytokine production in mast cells seems to be produced by other cells such as Th2 lymphocytes or basophils (22,30,32).…”

Section: Discussionmentioning

confidence: 90%

Human Intestinal Mast Cells Are Capable of Producing Different Cytokine Profiles: Role of IgE Receptor Cross-Linking and IL-4

Lorentz

Schwengberg

Sellge

et al. 2000

The Journal of Immunology

157

116

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Mast cells are recognized as a new type of immunoregulatory cells capable of producing different cytokines. So far, little is known about the cytokine profile of mature human mast cells isolated from intestinal tissue and cultured in the presence of stem cell factor (SCF). We observed that these cells express the proinflammatory cytokines TNF-α, IL-1β, IL-6, IL-8, IL-16, and IL-18 without further stimulation. Both IgE-dependent and IgE-independent agonists (e.g., Gram-negative bacteria) enhanced expression of TNF-α. Another set of cytokines consisting of IL-3, IL-5, IL-9, and IL-13 was expressed following activation by IgE receptor cross-linking. If mast cells were cultured in the presence of IL-4 and SCF, the production and release of IL-3, IL-5, and IL-13 was increased up to 4-fold compared with mast cells cultured with SCF alone. By contrast, IL-6 expression was completely blocked in response to culture with IL-4. In summary, our data show that mature human mast cells produce proinflammatory cytokines that may be up-regulated following triggering with IgE-independent agonists such as bacteria, whereas activation by IgE receptor cross-linking results in the expression of Th2-type cytokines. IL-4 enhances the expression of Th2-type cytokines but does not affect or even down-regulates proinflammatory cytokines.

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Section: Discussionmentioning

confidence: 90%

Human Intestinal Mast Cells Are Capable of Producing Different Cytokine Profiles: Role of IgE Receptor Cross-Linking and IL-4

Lorentz

Schwengberg

Sellge

et al. 2000

The Journal of Immunology

157

116

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“…However, removal of monocytes from atopic dermatitis patients" PBMC has been shown to give opposite results on IFN-'y production: in one report IFN-7 production was still low in the remaining cell population [31], while others showed that purified Tcells from atopic dermatitis patients produced even higher amounts of IFN-7 compared wilh normals [29], Possibly, Tcells are not ihe primary affected cells in atopy. Another ceil type might be a more important source of IL-4 in IgE responses, as is suggested for cells of the mast cell/basophil lineage [35][36][37].…”

Section: Discussionmentioning

confidence: 99%

IgE production in atopic patients is not related to IL-4 production

Kraan¹,

Aalberse²,

Aarden³

1994

Clinical and Experimental Immunology

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SUMMARYTo analy.se whether there is a general defect in T or B cell function in atopic individuals we have measured cytokine and IgE production by peripheral blood lymphocytes, isolated from 19 atopic donors (17 asthma/rhinitis and two dermatitis patients) in comparison with 19 non-atopic controls. After stimulation oflymphocytes with aiiti-CD2 and anti-CD28. we found no significant difference in IL-2, IL-4 and interferon-gamma (IEN--)) production. To examine the correlation between the production of IgE and IL-4, we stimulated lymphocytes with anti-CD2 and rIL-2. Under this condition both T eell iL-4 and B cell IgE production ean be measured. No significant diflerence was found for the amount of IgE and IL-4 produced between the two groups ( P > 005). The non-atopie donors showed a good correlation between IL-4 and IgE production (r = 0'70). Surprisingly, within the atopic group there was no correlation between IgE and IL-4 production at all (r = -0-04). The ratio of IgE to IL-4 was higher (although not signifieatitly) in the atopic group. Our data suggest that in atopic donors IgE production is less dependent on IL-4, and that other cytokines are involved.

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“…Histamine is a storage amine of mast cells and basophils. The proliferation of the precursor of both cells and the production of Ig E Abs are stimulated by Th2 cytokines such as IL-4, which are secreted by stimulated mast cells and basophils (51,52). Therefore, the effects of histamine on Th1 cytokine production may function as a negative feedback on excessive Th2 response.…”

Section: Discussionmentioning

confidence: 99%

Histamine Is a Potent Inducer of IL-18 and IFN-γ in Human Peripheral Blood Mononuclear Cells

Kohka

Nishibori²,

Ishibashi³

et al. 2000

The Journal of Immunology

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Histamine (10−7 to 10−4 M) concentration-dependently stimulated the production of IL-18 and IFN-γ and inhibited the production of IL-2 and IL-10 in human PBMCs. Histamine in the same concentration range did not induce the production of IL-12 at all. The stimulatory or inhibitory effects of histamine on cytokine production were all antagonized by H2 receptor antagonists ranitidine and famotidine in a concentration-dependent manner, but not by H1 and H3 receptor antagonists. Selective H2 receptor agonists, 4-methylhistamine and dimaprit, mimicked the effects of histamine on five kinds of cytokine production. The EC50 values of histamine, 4-methylhistamine, and dimaprit for the production of IL-18 were 1.5, 1.0, and 3.8 μM, respectively. These findings indicated that histamine caused cytokine responses through the stimulation of H2 receptors. All effects of histamine on cytokine responses were also abolished by the presence of either anti-IL-18 Ab or IL-1β-converting enzyme/caspase-1 inhibitor, indicating that the histamine action is dependent on mature IL-18 secretion and that IL-18 production is located upstream of the cytokine cascade activated by histamine. The addition of recombinant human IL-18 to the culture concentration-dependently stimulated IL-12 and IFN-γ production and inhibited the IL-2 and IL-10 production. IFN-γ production induced by IL-18 was inhibited by anti-IL-12 Ab, showing the marked contrast of the effect of histamine. Thus histamine is a very important modulator of Th1 cytokine production in PBMCs and is quite unique in triggering IL-18-initiating cytokine cascade without inducing IL-12 production.

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Human peripheral blood basophils primed by interleukin 3 (IL-3) produce IL-4 in response to immunoglobulin E receptor stimulation.

Cited by 361 publications

References 33 publications

Human Intestinal Mast Cells Are Capable of Producing Different Cytokine Profiles: Role of IgE Receptor Cross-Linking and IL-4

Human Intestinal Mast Cells Are Capable of Producing Different Cytokine Profiles: Role of IgE Receptor Cross-Linking and IL-4

IgE production in atopic patients is not related to IL-4 production

Histamine Is a Potent Inducer of IL-18 and IFN-γ in Human Peripheral Blood Mononuclear Cells

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