Induction of IgA-specific suppressor activity in human T-lymphocyte cultures

Sarfati, M; Rubio-Trujillo, M; Wong, K; Perry, John M.; Sehon, A.H.; Delespesse, Guy

doi:10.1016/0008-8749(85)90171-6

Cited by 20 publications

(30 citation statements)

References 19 publications

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“…35; unpublished data), IL-13 also upregulated expression of class II MHC antigen, sIgM, and CD72, which is the ligand for CD5 (41). Although the exact role of CD23 in the regulation of IgE synthesis remains to be determined, a strong correlation between CD23 expression and induction of IgE synthesis has been observed (13,(37)(38)(39), and soluble forms of CD23 have been found to enhance IgE synthesis (42). Since IL-13 induced significant expression of CD23 within 24 hr, our data also indicate that CD23 expression precedes IL-13-induced 6 switching, confirming the correlation between induction of CD23 expression and subsequent IgE synthesis.…”

Section: Discussionmentioning

confidence: 97%

Interleukin 13 induces interleukin 4-independent IgG4 and IgE synthesis and CD23 expression by human B cells.

Punnonen¹,

Aversa²,

Cocks³

et al. 1993

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

971

611

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Recently the cDNA encoding interleukin 13 (IL-13), a T-cell-derived cytokine, was cloned and expressed. The present study demonstrates that IL-13 induces IgG4 and IgE synthesis by human B cells. IL-13-induced IgG4 and IgE synthesis by unfractionated peripheral blood mononuclear cells and highly purified B cells cultured in the presence of activated CD4+ T cells or their membranes. IL-13-induced IgG4 and IgE synthesis is IL-4-independent, since it was not affected by neutralizing anti-IL-4 monoclonal antibody. Highly purified, surface IgD+ B cells could also be induced to produce IgG4 and IgE by IL-13, indicating that the production of these isotypes reflected IgG4 and IgE switching and not a selective outgrowth of committed B cells. IL-4 and IL-13 added together at optimal concentrations had no additive or synergistic effect, suggesting that common signaling pathways may be involved. This notion is supported by the observation that IL-13, like IL-4, induced CD23 expression on B cells and enhanced CD72, surface IgM, and class II major histocompatibility complex antigen expression. In addition, like IL-4, IL-13 induced germ-line IgE heavy-chain gene transcription in highly purified B cells. Collectively, our data indicate that IL-13 is another T-cellderived cytokine that, in addition to IL-4, efficiently directs naive human B cells to switch to IgG4 and IgE production.

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Section: Discussionmentioning

confidence: 97%

Interleukin 13 induces interleukin 4-independent IgG4 and IgE synthesis and CD23 expression by human B cells.

Punnonen¹,

Aversa²,

Cocks³

et al. 1993

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

971

611

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“…Recent experiments with mouse splenic lymphocytes indicated that IFN-y induces the formation of IgE-BF by normal T cells (17). To test the possibility that IL-4 or IFN-y may be involved in the induction of IgE-BF formation by T cells of HIV-1-infected (19). In rodent systems, however, fragments of Fc6R on B cells failed to bind to IgE (20).…”

Section: Resultsmentioning

confidence: 99%

Formation of IgE-binding factors by T cells of patients infected with human immunodeficiency virus type 1.

Carini

Margolick

Yodoi

et al. 1988

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

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Peripheral blood mononuclear cells of 10 out of 26 patients with human immunodeficiency virus type 1 (HIV-1) released IgE-binding factors, as determined by two independent assays. The formation of the factors by the mononudear cells was enhanced by incubation of the cells with homologous IgE. In the presence of IgE, peripheral blood mononuclear cells from 15 of the 26 patients formed a detectable amount of IgE-binding factors, whereas those of normal individuals or allergic rhinitis patients failed to do so. The major source of IgE-binding factors was the T cells of the HIV-1-infected patients. The CD8 + T cells from a HIV-1-infected patient formed IgE-binding factors upon incubation with IgE, and type II receptors for FcE were detected on both CD4' T cells and CD8' T cells in one of five patients studied.It was also found that culture supernatants of mononuclear cells from HIV-1-infected patients released soluble factors that induce normal human T cells to form IgE-binding factors. The results suggest that lymphocytes of some HIV-1-infected patients are activated to produce lymphokines regulating formation of IgE-binding factors.Previous experiments have shown that peripheral blood mononuclear cells (PBMCs) from ragweed-sensitive allergic individuals released soluble factors having affinity for IgE when the cells were incubated with allergen together with human IgE (1). Activation of normal PBMCs with phytohemagglutinin followed by incubation of the activated T cells with IgE also induced the formation of IgE-binding factors (IgE-BF). Young et al. (2) established FcE receptor-positive (FcR+) human T-cell clones from a patient with atopic dermatitis and found that these clones released IgE-BF.

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“…PWM was employed at the final concentration of 1/100, PHA-P and Con A were used at 1 and 25 yg/ml, respectively. EBV transformation was carried out exactly as described [6] by employing a titrated culture supernatant of the B95-8 marmoset cell line. For the preparation of T cell culture supernatants, 1 x lo6 T lymphocytes purified by two-cycle rosetting with AET-SRBC, were cultured for 48 h in 1 ml culture medium supplemented with either PWM, Con A or PHA; the supernatants were collected by centrifugation, passed through a 0.22-pm Millipore (Bedford, MA) filter and frozen at -20°C.…”

Section: Culture Conditionsmentioning

confidence: 99%

IgE receptors on human lymphocytes III. Expression of IgE receptors on mitogen‐stimulated human mononuclear cells

et al. 1986

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Human peripheral blood mononuclear cells (PBMC) were tested for the expression of Fc epsilon-receptor (Fc epsilon R) after stimulation with various mitogens in the absence of IgE. Fc epsilon R were found on virtually all the cells from 19 Epstein-Barr virus-transformed B cell lines including those derived from cord blood, from one agamma-globulinemic patient and VDS-0 pre-B cells. Hence, the data clearly indicate that Fc epsilon R may be expressed on very immature B cells. PBMC cultures stimulated with either pokeweed mitogen (PWM), phytohemagglutinin (PHA) or concanavalin A displayed an early increase of their content in Fc epsilon R-bearing cells followed by a decrease to levels below those of control cultures. After fractionation of the PWM-stimulated cultures into T and B cell-enriched preparations, most of the Fc epsilon R+ cells were in the in the B cell fractions and the same low levels of Fc epsilon R+ cells were found in the T cell fractions isolated from the PWM-stimulated and from the control cultures. Double-labeling experiments, employing biotinylated F(ab')2 monoclonal antibody to FcR and either fluorescein isothiocyanate-conjugated B1 or Mo2 monoclonal antibodies, indicated that PWM mainly exerted its effect on B cells and on monocytes. This effect was T cell dependent and it was mediated by soluble factors of T cell origin. At the peak of the PHA or concanavalin A response, most of the Fc epsilon R-bearing cells were found in the B cell fraction but the T cells isolated from mitogen-stimulated cultures contained significant more Fc epsilon R+ cells than those from the control cultures, suggesting that T cell mitogens had increased the expression of Fc epsilon R on some T cells. This view was supported by the finding of a higher proportion of Fc epsilon R+ cells in PHA-stimulated than in control cultures of highly purified T cells with a maximum response at the end of the culture period. Double-labeling experiments at the peak (day 2) of the peripheral blood mononuclear cell response indicated that the expression of Fc epsilon R was increased on B cells (B1+) and on monocytes (Mo2+). By using the same approach at the peak of the T cell response (day 7), it was found that T cells isolated from PHA-stimulated cultures expressed more Fc epsilon R than those isolated from control cultures.(ABSTRACT TRUNCATED AT 400 WORDS)

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Induction of IgA-specific suppressor activity in human T-lymphocyte cultures

Cited by 20 publications

References 19 publications

Interleukin 13 induces interleukin 4-independent IgG4 and IgE synthesis and CD23 expression by human B cells.

Interleukin 13 induces interleukin 4-independent IgG4 and IgE synthesis and CD23 expression by human B cells.

Formation of IgE-binding factors by T cells of patients infected with human immunodeficiency virus type 1.

IgE receptors on human lymphocytes III. Expression of IgE receptors on mitogen‐stimulated human mononuclear cells

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