Expression of Lymphocytes FcεRII/CD23 in Allergic Children Undergoing Hyposensitization

Gagro, Alenka; Rabatić, Sabina; Trešćec, Anđa; Dekaris, Dragan; Medar-Lasić, Maja

doi:10.1159/000236520

Cited by 30 publications

(25 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, enhanced allergen uptake by monocytes and enhanced T cell proliferation might be beneficial in terms of improv ing the efficiency of immunotherapy [37], The change in the expression of CD23 on B lymphocytes during RIT, and its possible correlation with allergen-specific IgE and IgG4, as well as the clinical benefit of immunotherapy has been incompletely investigated. However, a significant decrease in CD20+CD23+ lymphocytes was reported in allergic chil dren after 6 weeks of standard hyposensitization [38]. A similar finding was observed in patients with atopic dermat itis [39], They had an increased number of CD23+ B cells which correlated to the severity of a disease.…”

Section: Discussionsupporting

confidence: 63%

Decrease in CD23+ B Lymphocytes and Clinical Outcome in Asthmatic Patients Receiving Specific Rush Immunotherapy

Kljaić-Turkalj¹,

Čvoriščec²,

Tudorić³

et al. 1996

Int Arch Allergy Immunol

Self Cite

View full text Add to dashboard Cite

Rush immunotherapy (RIT) has been documented as useful in the treatment of patients with allergic bronchial asthma. To investigate the mechanisms of its action, we studied changes in the serum levels of total IgE, allergen-specific IgE and IgG4, and expression of CD23 on peripheral blood B cells in patients receiving RIT. Twenty patients with perennial bronchial asthma were evaluated before the beginning of RIT, as well as 6 weeks and 6 months later. Compared to pre-treatment values, the level of Der-p-specific IgG4 and IgE significantly increased after 6 weeks and 6 months of RIT, while the total serum IgE remained unchanged. Furthermore, after 6 months of RIT, the percentage of CD23+ B cells and its CD23 receptor density significantly decreased. Since the symptom score improved and the need for medication decreased, we evaluated RIT as a useful procedure. After 6 months, 30% of patients did not have an asthma attack, with no medication in the last month, while 10% of them were asthma free for the last 3 months. No significant correlation between the clinical improvement, and in vitro changes was found. Furthermore, the observed in vitro changes were not significantly different in patients who responded with clinical improvement, compared to those with unchanged intensity of asthma. In conclusion, during specific RIT we found a significant increase in Der-p-specific IgE and IgG4 antibodies, as well as a moderate decrease in CD23+ B cells and its CD23 receptor density. These findings suggest a change in the lymphokine profile of patients receiving specific immunotherapy, and that the inhibition of IL-4-induced B cell stimulation may be hypothesized as the most important mechanism.

show abstract

Section: Discussionsupporting

confidence: 63%

Decrease in CD23+ B Lymphocytes and Clinical Outcome in Asthmatic Patients Receiving Specific Rush Immunotherapy

Kljaić-Turkalj¹,

Čvoriščec²,

Tudorić³

et al. 1996

Int Arch Allergy Immunol

Self Cite

View full text Add to dashboard Cite

show abstract

“…1c), while CD23® was not found to be significantly elevated. It was already shown using flow cytometry that atopic patients have a higher percentage of Fc²RII/CD23 lymphocytes than healthy controls [25,26]. It may be possible that CD23® is involved in B cell activation and differentiation, while CD23¯could play a role in the T cell-dependent responses to allergens [27].…”

Section: Discussionmentioning

confidence: 98%

Spontaneous CD30 mRNA expression in peripheral blood mononuclear cells from atopic patients with high IgE serum levels

Esnault¹,

Benbernou

Lavaud

et al. 1996

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SUMMARYCD30 is a surface molecule which can be expressed by normal B and T lymphocytes. Our study focused on the CD30 expression and release compared with IL-4 expression as well as CD23-®/¯in peripheral blood mononuclear cells (PBMC) from atopic subjects and controls. Data showed a lack of CD30 mRNA expression in the PBMC of control subjects, while it was significantly expressed in those of 6/11 atopic patients. No substantial amounts of spontaneous soluble CD30 (sCD30) could be detected by ELISA in both atopic and control groups. Interestingly, CD30 mRNA expression in PBMC of allergic patients was positively correlated with IgE serum levels (r 0 . 79, P 0 . 003). Studies on purified B cells showed that CD30 was expressed mainly in CD19 B cells of allergic patients. These data suggest highly a potential functional significance of the CD30 molecule in IgE response during allergic diseases.

show abstract

“…cDNA was synthesized by using 2.5 g of total RNA isolated from the samples. The cDNA was primed with oligo(dT) [12][13][14][15][16][17][18] and with random hexamer nucleotides (N6) in the absence of signal from the former method. The Fc receptor primers used for PCR were based on the published sequences of the human Fc␥ -RI, -RII, -RIII, and FcRII genes (25,26) and included the following primer sets: Fc␥RI: 5Ј primer, 5Ј-ATGTGGTTCTTGACAAC-TCTGCTC-3Ј and 3Ј primer, 5Ј-ATGTCTGTCTTCTTGAAG-GCTGGA-3Ј; Fc␥RIIA,C: 5Ј primer, 5Ј-GACTCCATTCAGT-GGTTCCA-3Ј; and 3Ј primer: 5Ј-GTCAGCTGTTTCATAGT-CATTG-3Ј; Fc␥RIIB: 5Ј primer, 5Ј-GACTCCATTCAGTGGT-TCCA-3Ј and 3Ј primer, 5Ј-CCCAACTTTGTCAGCCTCATC-3Ј; Fc␥RIII: 5Ј primer, 5Ј-AAGATCTCCCAAAGGCTGTG-3Ј and 3Ј primer, 5Ј-ATGGACTTCTAGCTGCACCG-3Ј; FcRII: 5Ј primer, 5Ј-CGTCTCTCAAGTTTCCAAG-3Ј and 3Ј primer: 5Ј-GCACTTCCGTTGGAATTTG-3Ј.…”

Section: Methodsmentioning

confidence: 99%

“…Accordingly, immune complex͞Fc receptor interactions potentially underlie the progression of the airway inflammatory and bronchoconstrictor responses in asthma, wherein the immediate bronchoconstriction accompanying antigen exposure is followed by the development of the late phase asthmatic response involving various proinflammatory cells. Indeed, recent studies have demonstrated that expression of the inducible form of the low affinity IgE receptor (FcRII or CD23) is up-regulated on monocytes and alveolar macrophages (14), as well as on circulating B lymphocytes (15,16) isolated from atopic asthmatic subjects.…”

mentioning

confidence: 99%

Autologously up-regulated Fc receptor expression and action in airway smooth muscle mediates its altered responsiveness in the atopic asthmatic sensitized state

Hákonarson

Grunstein²

1998

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

View full text Add to dashboard Cite

To elucidate the role of IgE-dependent mechanisms in inducing altered airway responsiveness in the atopic asthmatic state, the expression and actions of Fc receptor activation were examined in isolated rabbit tracheal smooth muscle (TSM) tissue and cultured cells passively sensitized with sera from atopic asthmatic patients or nonatopic͞ nonasthmatic (control) subjects. Relative to control tissues, the atopic asthmatic-sensitized TSM exhibited significantly increased maximal isometric contractility to acetylcholine (P < 0.01) and attenuated maximal relaxation responses and sensitivity (i.e., ؊log ED 50 ) to isoproterenol (P < 0.005). These changes in agonist responsiveness in atopic sensitized TSM were ablated by pretreating the tissues with a blocking mAb to the low affinity receptor for IgE, FcRII (i.e., CD23) or by depleting the sensitizing serum of its immune complexes. Moreover, in complimentary experiments, exogenous administration of IgE immune complexes to naive TSM produced changes in agonist responsiveness that were qualitatively similar to those obtained in the atopic asthmatic-sensitized state. Extended studies further demonstrated that, in contrast to their respective controls, atopic asthmatic serum-sensitized human and rabbit TSM tissue and cultured cells exhibited markedly induced mRNA and cell surface expression of FcRII, whereas constitutive expression of the IgG receptor subtype, Fc␥RIII, was unaltered. Finally, the up-regulated mRNA expression of FcRII observed following exposure of TSM to atopic asthmatic serum or to exogenously administered IgE immune complexes was significantly inhibited by pretreating the tissues or cells with anti-CD23 mAb. Collectively, these observations provide evidence demonstrating that the altered agonist responsiveness in atopic asthmatic sensitized airway smooth muscle is largely attributed to IgEmediated induction of the autologous expression and activation of FcRII receptors in the airway smooth muscle itself.Bronchial asthma is characterized by airways inflammation, exaggerated airway reactivity to bronchoconstrictor agonists, and attenuated ␤-adrenoreceptor-mediated airway relaxation (1-3). In individuals with atopic asthma, mast cell activation has been implicated in mediating the immediate bronchoconstrictor response acutely following antigen inhalation, a process involving IgE-mediated activation of the high affinity IgE receptor (FcRI), leading to cellular degranulation and the release of various mast cell-derived mediators (4-6). The identification of Fc receptors on other cell types in the lung (e.g., mononuclear cells, eosinophils, and dendritic cells) suggests that, apart from mast cells per se, these other cell types may also serve to propagate the pro-inflammatory allergic pulmonary response, most likely via the orchestrated extended release of various cytokines (7-13). Accordingly, immune complex͞Fc receptor interactions potentially underlie the progression of the airway inflammatory and bronchoconstrictor responses in asthma, wherein the i...

show abstract

Expression of Lymphocytes FcεRII/CD23 in Allergic Children Undergoing Hyposensitization

Cited by 30 publications

References 25 publications

Decrease in CD23+ B Lymphocytes and Clinical Outcome in Asthmatic Patients Receiving Specific Rush Immunotherapy

Decrease in CD23+ B Lymphocytes and Clinical Outcome in Asthmatic Patients Receiving Specific Rush Immunotherapy

Spontaneous CD30 mRNA expression in peripheral blood mononuclear cells from atopic patients with high IgE serum levels

Autologously up-regulated Fc receptor expression and action in airway smooth muscle mediates its altered responsiveness in the atopic asthmatic sensitized state

Contact Info

Product

Resources

About