Factors Influencing Human IgE Synthesis in vitro and in vivo

Weck, A.L. de; Stadler, Beda M.; Knutti-Müller, J.; Ruff, Paul; Hofstetter, H.; Lüdin, C.; Heusser, Christoph

doi:10.1159/000233750

Cited by 10 publications

(2 citation statements)

References 9 publications

(16 reference statements)

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“…PWM) to induce IgE production by B cells from normal or atopics [3,8,171. Until recently, many investigations focused on the induction of in vitro IgE synthesis by lectins in human PBL cultures.…”

Section: Discussionmentioning

confidence: 99%

induction of human in vitro ige synthesis via stimulation by anti‐cd3 antibody

1988

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Mitogens such as pokeweed mitogen, Staphylococcus aureus Cowan I, concanavalin A and phytohemagglutinin and monoclonal anti-CD antibodies were examined for their capacity to induce IgE synthesis by peripheral blood leukocytes obtained from both atopic and nonatopic individuals. While lectins failed to induce IgE synthesis, monoclonal anti-CD3 antibodies were very potent stimuli for the induction of human in vitro IgE synthesis, possibly due to the activation of T cells. Activation via CD4 or CD8 molecules by OKT4 or OKT8 antibodies did not lead to a T cell-dependent modulation of IgE synthesis. PWM acted in synergy with the enhancing effect of anti-CD3 antibodies for IgE synthesis. In vitro IgG production was less affected. These results indicate that activation of T cell via CD3 molecules may be important in the regulation of IgE immune responses in man. Furthermore, the successful induction of IgE synthesis by anti-CD3 antibody in unfractionated peripheral blood leukocytes culture provides a simple model for investigation of human IgE regulatory mechanism in vitro.

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Section: Discussionmentioning

confidence: 99%

induction of human in vitro ige synthesis via stimulation by anti‐cd3 antibody

1988

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“…There have been numerous reports (17,52,53,58,79,80,113,143, 144) of human FCER+ T-cell lines and hybridomas with TH inducer activity that release IgEBF with biochemical properties similar to those described for rodent IgE potentiating factors and that act on preactivated IgE-bearing B cells. There is also increasing evidence that human T-cell lines can produce either potentiating or suppressive IgEBF that differ only in their carbohydrate moieties depending on the culture conditions (53,58,112).…”

Section: Isotype-specijic Regulation Of Ige Synthesismentioning

confidence: 99%

Regulation of IgA Expression by Isotype-Specific T Cells and Soluble Binding Factors

Word¹,

Crago²,

Tomasi³

1986

Annu. Rev. Microbiol.

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The data presented here suggest a model for isotype-specific regulation of IgA synthesis by Fc alpha R+ T cells (Figure 1). Immature mIgM+ +/- mIgD+ B cells are induced by T switch cells to express cell surface IgA (a phenotypic switch). If the T switch cell induces mIgA expression via a long primary RNA transcript from an unrearranged C alpha allele, the hypothetical intermediate switch B cell results (step 1); this may be the mechanism of heavy chain expression in memory B cells that express low levels of Ig. Alternatively, T switch cells may induce a DNA rearrangement in the CH locus of the B cell (a genotypic switch), which results in a deletion of all CH loci except C alpha (step 2). TH inducer cells promote maturation of mIgA+ B cells to IgA-secreting plasma cells. This may involve a DNA switch rearrangement (step 3) or the maturation of previously switched cells (step 4), and appears to be mediated via an IgABF with enhancing activity. Not shown in this figure, but inherent in this model, is a suppressive regulatory arm that may be mediated via IgABF with suppressive activity released from Fc alpha R+ suppressor T cells. Due to the presence of Fc alpha R on a variety of cell types, IgABF may suppress synthesis of IgA by acting not only on mIgA+ B cells but also on regulatory cells (T cells, B cells, and macrophages) bearing IgA bound to Fc alpha R. If the IgA system is analogous with the IgE system, mIgA-bearing B cells may be the direct target of IgABF. Binding of Ig to FcR has been shown to (a) increase the number of Fc receptors per cell, (b) enhance the number of cells expressing Fc receptors, (c) induce the release of IgBF that either suppress or enhance Ig secretion, and (d) effectively convert surface Ig- cells into surface Ig+ cells that are therefore receptive to IgBF. Thus, FcR+ cells may interact with IgBF and Ig via a regulatory network to stimulate or inhibit the immune response in an isotype-specific manner. Cell surface molecules (mIg, FcR) may serve as sensors that allow the cell to detect and respond to fluctuations in the levels of immune mediators that serve to modulate Ig synthesis and secretion. The relationship between IgBF and FcR is not known, nor is it known whether Fc receptors expressed by different cell types are encoded by the same gene and are controlled similarly.(ABSTRACT TRUNCATED AT 400 WORDS)

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Characterization of human T cell‐derived IgE‐potentiating factor

et al. 1986

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We have previously shown that Fc epsilon receptor-positive (Fc epsilon R+) T cell lines from patients with the hyper IgE syndrome secrete IgE-binding factors which selectively enhance IgE but not IgG synthesis in cultures of B cells obtained from patients with allergic rhinitis but not from nonatopic subject. In the present study we have tested the effect of supernatants from Fc epsilon R+ T cell lines on a large panel of B cells from atopic patients (n = 20). We found that IgE synthesis was selectively enhanced only in B cell cultures in which there was ongoing spontaneous synthesis of IgE. The target of IgE-potentiating factor(s) was a large low-density B cell present in the circulation of responding atopic donors. In addition, we further characterized IgE-potentiating factors derived from Fc epsilon R+ T cell lines. The factor(s) fractionated into 2 peaks on Sephadex G-75 with approximate molecular masses of 15,000 and 60,000 kDa, and had affinity for lentil lectin but not for peanut agglutinin. Release of IgE-potentiating factor(s) was enhanced by the addition of exogenous human IgE to Fc epsilon R+ T cell cultures and was inhibited by tunicamycin, an inhibitor of N-glycosylation. These studies suggest a close homology between the physicochemical characteristics of human and rodent IgE-potentiating factors and the immune signals which modulate production of these IgE regulatory factors.

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Factors Influencing Human IgE Synthesis in vitro and in vivo

Cited by 10 publications

References 9 publications

induction of human in vitro ige synthesis via stimulation by anti‐cd3 antibody

induction of human in vitro ige synthesis via stimulation by anti‐cd3 antibody

Regulation of IgA Expression by Isotype-Specific T Cells and Soluble Binding Factors

Characterization of human T cell‐derived IgE‐potentiating factor

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