Human IgE-binding factors

doi:10.1016/0167-5699(89)90173-4

Immunology Today

Volume 10, Issue 5, May 1989, Pages 159-164

Immunology Today

https://doi.org/10.1016/0167-5699(89)90173-4 Get rights and content

Abstract

The production of IgE antibodies is known to be regulated by isotype-specific mechanisms that are not antigen specific. During the last decade several studies have indicated that soluble factors with affinity for IgE (IgE-binding factors, IgE-BFs) may exert such a role by interacting with IgE-bearing B lymphocytes. In the human, some of these IgE-BFs appear to be identical to soluble CD23, a B-cell surface marker thought to be involved in the control of B-cell proliferation or differentiation. In this article, Guy Delespesse and colleagues summarize several new findings regarding the cellular origin, structure and function of IgE-BFs/sCd23.

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Cited by (117)

Identification of new phosphorylation sites of CD23 in B-cells of patients with chronic lymphocytic leukemia
2018, Leukemia Research
Citation Excerpt :
Two isoforms of CD23 (CD23a and CD23b) have been described, which differ in their intracytoplasmic domains, and are linked to different signaling events [11]. CD23a is restrictively expressed on antigen activated B-cells, while CD23b is subjected to up-regulation following Epstein-Barr virus infection, stimulation by IL-4 in B cells or monocytes, or by engagement of CD40 on B cells, as well as also being inducible on a subset of T cells, polymorphonuclear leucocytes, follicular dendritic cells, intestinal epithelial cells and bone marrow stromal cells [7,12]. Both, CD23a and CD23b isoforms are expressed by malignant B cells.
B-cell chronic lymphocytic leukemia (B-CLL) is the most common lymphoproliferative disorder in adults. Patients with B-CLL strongly express the CD23 – C type of lectin (low affinity IgE receptor, Fc epsilon RII), which is linked to B cell activation and proliferation. Phosphorylation in lymphocytes is tightly associated with regulation of protein activities, functional regulation and cell signaling, and may thus affect initiation and/or progression of the disease. Here we report changes in the phosphorylation of CD23 on threonine (pThr314) and two serine residues (pSer254, pSer265) in B lymphocytes of B-CLL patients, using a flow cytometry approach. The majority of tested patients with active forms of B-CLL presented a notable overexpression of CD23 along with pThr314, pSer254, and pSer265 CD23 phosphorylation positivity. Moreover, we have experimentally stimulated the CD23 phosphorylations in a subset of peripheral blood lymphocytes of healthy controls by phorbol-12-myristate-13-acetate treatment. This affects the activation of competent phosphorylation mediating kinases, resulting in the enhanced phosphorylation pattern. Together, these data confirm that CD23 protein is phosphorylated in B cells of B-CLL patients, report the identification of new CD23 phosphorylation sites, and suggest a possible role(s) of such phosphorylations in the activation of CD23 during the process of lymphocytic activation in B-CLL.
High expression of CD23 in the proliferation centers of chronic lymphocytic leukemia in lymph nodes and spleen
1999, Human Pathology
Chronic lymphocytic leukemia (CLL) is a B-cell neoplasm composed of a heterogeneous mixture of cells, including small lymphocytes, prolymphocytes, and large transformed cells; these last cells appear to represent the proliferating compartment. CLL cells express, in addition to B cell markers, the transmembrane receptor CD23. CD23 functions as the receptor for IgE and also appears to play a role in controlling the growth and proliferation of lymphocytes. Its level of expression among the different cells in CLL has not been examined. In this study, we show that CD23 expression is much higher in the large transformed CLL cells than in the small lymphoid population. This may provide an explanation for the observed correlation between a circulating CD23 cleavage product (soluble CD23) and prognosis in CLL. In addition, we have shown that proliferation in splenic CLL occurs preferentially in the white pulp zones, even in cases in which both the white and red pulp are extensively infiltrated.
Allergie et cytokines
1998, Annales de l'Institut Pasteur/Actualites
L'allergie désigne un état d'hypersensibilité dont le mécanisme initial appartient à une réponse immunitaire normale, mais qui, sous l'effet de multiples facteurs, est mal contrôlée et déséquilibrée. Parmi les facteurs qui vont créer cet emballement du système immunitaire avec une réponse exacerbée, les cytokines jouent un rôle essentiel dans l'établissement de cette hypersensibilité et de son expression démesurée qui conduit à la pathologie inflammatoire d'origine allergique.
Cell-mediated immunity in allergic bronchopulmonary aspergillosis
1998, Immunology and Allergy Clinics of North America
Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity lung disease mediated by an allergic late-phase inflammatory response to Aspergillus fumigatus antigens characterized by markedly elevated allergen specific and total immunoglobulin E (IgE) levels and eosinophilia, and manifested by wheezing, pulmonary infiltrates, and pulmonary bronchiectasis and fibrosis. ABPA afflicts only a small percentage of susceptible atopic individuals with either asthma or cystic fibrosis (CF). ABPA is unique in that it is caused by A. fumigatus, a living fungus growing within the mucosal lumen of the bronchi that releases a multitude of proteins whose biologic function alters the host immune responses in addition to being immunogenic. Elucidation of the immunopathogenesis of ABPA has provided valuable information related to allergen-induced chronic asthma. More recently, immunogenetic studies have further contributed to the understanding of the immunopathogenesis of why certain individuals are susceptible to develop ABPA. Immunologic responses to Aspergillus, as well as to other microorganisms, may be categorized as either T helper (Th)1 or Th2 CD4+ T-cell responses. 61, 110, 128 Th1 CD4+ T-cell cytokines, such as interferon gamma (IFN-γ), interleukin 2 (IL-2), and tumor necrosis factor (TNF)-β, enhance cytotoxic and macrophage activity (e.g., cellular immunity), whereas Th2 CD4+ T-cell cytokines, such as IL-4, IL-5, IL-10, and IL-13, promote antibody synthesis (e.g., humoral antibody immunity) (Table 1). It is hypothesized that protective host immunity to A. fumigatus is a Th1 CD4+ T-cell response, whereas a Th2 CD4+ T-cell humoral response found in ABPA is nonprotective and leads to a hypersensitivity pulmonary lung disease.
In vitro release of soluble CD23 by human lymphocytes in ragweed-sensitive versus nonatopic patients following stimulation with ragweed antigen E
1996, Annals of Allergy, Asthma and Immunology
Soluble CD23 is the proteolytic cleavage product of the low affinity receptor (FcERII). Functions of CD23 and its soluble products may include upregulation of IgE production and stimulation of B lymphocyte growth.
Soluble CD23 was quantitated in supernatants of lymphocytes from nine ragweed-sensitive and eight nonatopic subjects stimulated in vitro by antigen E (amb A1), crude ragweed extract, and pokeweed mitogen (PWM).
Although PWM stimulation produced no significant difference between groups, sCD23 release was significantly elevated in the cells of nontoxic patients stimulated with antigen E and crude ragweed extract. (P < .05).
This finding supports the concept of separate pathways of activation by antigen and mitogen for sCD23 release and suggests ragweed-sensitive and nonatopic patients have fundamental differences in the response of sCD23 release to ragweed antigen stimulation.
Role of CD23 in NO production by human monocytic cells
1995, Research in Immunology

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reviewsHuman IgE-binding factors

Abstract

J. Mol. Biol.

J. Biol. Chem.

J. Biol. Chem.

Cell

Cell. Immunol.

Annu. Rev. Immunol.

J. Exp. Med.

Prog. Allergy

J. Exp. Med.

J. Immunol.

Int. Rev. Immunol.

Int. Rev. Immunol.

Cell

EMBO J.

Immunology

J. Immunol.

J. Immunol.

Eur. J. Immunol.

Adv. Immunol.

Eur. J. Immunol.

J. Exp. Med.

Nucleic Acids Res.

Biochemistry

J. Exp. Med.

reviews
Human IgE-binding factors