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

Delespesse, Guy; Sarfati, M; Rubio-Trujillo, M; Wolowiec, Terry

doi:10.1002/eji.1830160903

Cited by 29 publications

(13 citation statements)

References 14 publications

(6 reference statements)

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“…Results similar to ours have been obtained with B lymphocytes [21,35]. Moreover, Delespesse et al [36] found evidence that IgE protects FceRII from prote olysis; they have also recently described a FceRI ¡-as sociated proteolytic activity [37].…”

Section: Discussionsupporting

confidence: 76%

Regulation of the Expression of the Low-Affinity IgE Receptor (FcεRII) in the Human Monocyte-Like Cell Line U-937 by Phorbol Esters and IgE

Pucillo

Salzano

Pepe

et al. 1990

Int Arch Allergy Immunol

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The expression of the low-affinity receptor for IgE FcεRII) in the human monocyte-like U-937 cell line can be upregulated by the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) and by IgE. TPA induces terminal differentiation of U-937 cells and causes a four- to fivefold increase in the number of FcεRII. TPA also modulates the expression of several other membrane markers of U-937 cells. IgE alone has a modest effect on the expression of FcεRII (about a 10% increase), while simultaneous treatment of U-937 cells with TPA and IgE has a cooperative effect, causing an eightfold increase in the number of FcεRII. Cycloheximide strongly suppresses the expression of FcεRII, both in TPA-stimulated and unstimulated cells; this effect can be partly reversed by culturing the cells in the presence of IgE. These results suggest that TPA induces the expression of newly synthesized receptors, while IgE causes an accumulation of preformed receptors.

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Section: Discussionsupporting

confidence: 76%

Regulation of the Expression of the Low-Affinity IgE Receptor (FcεRII) in the Human Monocyte-Like Cell Line U-937 by Phorbol Esters and IgE

Pucillo

Salzano

Pepe

et al. 1990

Int Arch Allergy Immunol

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“…Inasmuch as an increase in the percentage o f .~c e~( + j cells b a s observed only in allergic younger children (0-2 yr) in whom intensive sensitization might be occurring, it may be a reaction related to this sensitization. Activation of T cells by allergens during the sensitizing process may cause the increase in FctR(+) cells because FctR was induced on lymphocytes by soluble factors secreted by activated T cells (10)(11)(12). Additional investigation is required in order to confirm this assumption.…”

Section: Discussionmentioning

confidence: 99%

IgE Receptor-Bearing Lymphocytes in Allergic and Nonallergic Children

et al. 1988

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ABSTRACT. Using a monoclonal anti-human IgE receptor (FctR) antibody, the percentage of FctR(+) cells among peripheral blood lymphocytes in children with or without allergic disorders was determined. The percentage of FctR(+) cells in 63 nonallergic children was 4.3 2 1.5%, which did not vary with age and was equal to that of adults (4.2 + 1.2%). Allergic younger children (0-2 yr) showed a significantly higher percentage of FctR(+) cells (7.7 f 3.0%) than nonallergic younger children (0-2 yr) (4.0 + 1.3%, p < 0.001). Similarly, in allergic younger children, serum IgE levels (geometric mean = 58.9 IU/ml) were also significantly higher than those of nonallergic younger children (geometric mean = 2.0 IU/ml) (p < 0.01). A positive correlation between the percentages of FctR(+) cells and serum IgE levels was observed (Spearman rank = 0.88, p < 0.01)) in eight allergic younger children (0-2 yr) with serum IgE levels higher than 100 IU/ml. The increase in the percentage of FUR(+) cells in allergic younger children (0-2 yr) was not a secondary phenomenon caused by serum IgE because serum IgE levels in these children were much lower than the concentration at which IgE enhance FctR expression on lymphocytes. In conclusion, FctR(+) lymphocytes may play a regulatory role in IgE synthesis in allergic younger children (0-2 yr). (Pediatr Res 24: 254-257,1988

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“…Upon incubation at 37°C, freshly isolated and highly purified B lymphocytes rapidly loose their FctR II [11]; this is associated with the disappearance of Fc(;R II mRNA and the release of IgE-BFs in the culture supernatant [12]. Further studies showed that the disappearance of surface FcfR II was not due to their internalization, but rather to their shedding.…”

Section: Regulation Of Fc R II Expressionmentioning

confidence: 99%

“…Further studies showed that the disappearance of surface FcfR II was not due to their internalization, but rather to their shedding. The latter was significantly reduced by incubating the cells with IgE [11], whereas it was increased by pretreat ment of the cells with inhibitors of N-linked glycosylation like tunicamycin, swaisonine, and castanospermine [Letellier and Delespesse, unpubl. observations].…”

Section: Regulation Of Fc R II Expressionmentioning

confidence: 99%

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Human Fc<sub>ε</sub>R II and IgE-Binding Factors

Delespesse

Sarfati

Hofstetter

et al. 1989

Int Arch Allergy Immunol

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The low-affinity receptor for IgE (Fc_εR II) is mainly expressed on B lymphocytes, although it may also be found on some monocytes, eosinophils, and platelets. The presence of Fc_εR II on T cells is still controversial, but our results demonstrate that it is expressed on some HTLV-I-transformed T lymphocytes, and they strongly suggest that it may be found on a small proportion of normal T cells. Fc_εR II is a 45-KD glycoprotein containing one N-linked carbohydrate of complex type, O-linked carbohydrates, and sialic acid residues. Fc II is cleaved into soluble fragments with molecular weights of 37, 33, 25, and 12 KD, the first three retain the ability of binding to IgE, i.e., they are IgE-binding factors (IgE-BFs). The enzymes involved in their proteolytic cleavage are cell bound. The cDNA coding for Fc_εR II was cloned and functionally expressed. The predicted sequence has no homology with that of murine IgE-BFs which are of T cell origin. However, there is a striking homology with several animal lectins, and since the IgE-binding site is located in the homology region, it is possible that it binds to IgE via the carbohydrates expressed on the Fc region of this immunoglobulin. The expression of Fc_εR II on B cells and the release of IgE-BFs are upregulated by interleukin 4 and suppressed by gamma and alpha interferons. The finding that Fc_εR II is identical to CD23, known as a B cell activation marker, suggests that Fc_εR II or its soluble fragments are involved in B cell activation. Accumulating evidence suggests that some soluble fragments of Fc_εR II display B cell growth factor activity. Finally, several observations strongly suggest that IgE-BFs regulate human IgE synthesis.

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

Cited by 29 publications

References 14 publications

Regulation of the Expression of the Low-Affinity IgE Receptor (FcεRII) in the Human Monocyte-Like Cell Line U-937 by Phorbol Esters and IgE

Regulation of the Expression of the Low-Affinity IgE Receptor (FcεRII) in the Human Monocyte-Like Cell Line U-937 by Phorbol Esters and IgE

IgE Receptor-Bearing Lymphocytes in Allergic and Nonallergic Children

Human Fc<sub>ε</sub>R II and IgE-Binding Factors

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