Mechanisms of allergen-specific desensitization

Uermösi, Christina; Beerli, Roger R.; Bauer, Monika; Manolova, Vania; Dietmeier, Klaus; Buser, Regula B.; Kündig, Thomas M.; Saudan, Philippe; Bachmann, Martin F.

doi:10.1016/j.jaci.2010.05.040

Cited by 87 publications

(115 citation statements)

References 38 publications

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“…Immune complexes made of allergen and autologous Abs improved allergy to grass pollen (58). Supporting this in vivo observation, IgG anti-allergen Abs were reported to inhibit allergen-induced basophil activation (20,59). With this system, Cady et al (20) found that FcgRIIA was required for inhibition.…”

Section: Discussionmentioning

confidence: 91%

Fcγ Receptors Inhibit Mouse and Human Basophil Activation

Cassard

Jönsson²,

Arnaud³

et al. 2012

The Journal of Immunology

118

120

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Besides high-affinity IgE receptors (FcεRI), human basophils express activating (FcγRIIA) and inhibitory (FcγRIIB) low-affinity IgG receptors. IgG receptors (FcγR) were also found on mouse basophils, but not identified. We investigated in this study FcγR and the biological consequences of their engagement in basophils of the two species. We found the following: 1) that mouse basophils also express activating (FcγRIIIA) and inhibitory (FcγRIIB) low-affinity FcγR; 2) that activating FcγR can activate both human and mouse basophils, albeit with different efficacies; 3) that negative signals triggered by inhibitory FcγR are dominant over positive signals triggered by activating FcγR, thus preventing both human and mouse basophils from being activated by IgG immune complexes; 4) that the coengagement of FcεRI with inhibitory and activating FcγR results in a FcγRIIB-dependent inhibition of IgE-induced responses of both human and mouse basophils; 5) that FcγRIIB has a similar dominant inhibitory effect in basophils from virtually all normal donors; and 6) that IL-3 upregulates the expression of both activating and inhibitory FcγR on human basophils from normal donors, but further enhances FcγRIIB-dependent inhibition. FcγR therefore function as a regulatory module, made of two subunits with antagonistic properties, that prevents IgG-induced and controls IgE-induced basophil activation in both mice and humans.

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Section: Discussionmentioning

confidence: 91%

Fcγ Receptors Inhibit Mouse and Human Basophil Activation

Cassard

Jönsson²,

Arnaud³

et al. 2012

The Journal of Immunology

118

120

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“…The specific IgE level in those animals reached the same level of sensitized mice that were not orally challenged with OVA, but the difference between these two groups regarding the humoral response is in the concentration of specific IgG1. It has been shown that beyond neutralization, IgG (IgG1 in mice and IgG4 in humans) blocks mast cell activation [25] and can even protect IgE-mediated anaphylaxis [26]. Indeed, this is one of the explanations of why the IgE levels do not necessarily decrease during oral immunotherapy despite showing efficiency, both in humans and in murine experimental models [22,23,27].…”

Section: Discussionmentioning

confidence: 99%

Prolonged ingestion of ovalbumin diet by sensitized mice improves the metabolic consequences induced by experimental food allergy

Batista¹,

Pereira²,

Noviello³

et al. 2014

Clinical and Experimental Immunology

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SummaryThe prevalence of food allergy is rising in the western world. Allergen restriction is the chosen treatment in this condition, but continuous ingestion of the antigen has shown positive results in clinical trials. In a previous study, we have shown several allergic and metabolic alterations after 7 days of ovalbumin (OVA) ingestion by sensitized mice. The aim of this study was to investigate whether prolonged ingestion of antigen by sensitized mice would reverse the metabolic consequences caused by experimental food allergy. For this, allergic and metabolic parameters were analysed after prolonged ingestion of an OVA diet by OVA-sensitized mice. As shown previously, after 7 days of OVA consumption, sensitized mice showed increased serum levels of anti-OVA immunoglobulin (Ig)E and IgG1, aversion to the antigen ingestion, marked body and adipose tissue weight loss, followed by adipose tissue inflammation and decreased serum levels of adipokines, glucose and triglycerides. However, after 14 days of oral challenge, sensitized mice showed an anti-OVA IgE level similar to the mice that were only sensitized, but the specific IgG1 did not change. With this prolonged ingestion of OVA, sensitized mice were protected from OVA-induced anaphylaxis when the antigen was given systemically at a dose of 2 mg/animal. Moreover, various parameters analysed were significantly ameliorated, including adipose tissue inflammation, body and adipose tissue loss, as well as serum levels of adipokines and triglycerides. Therefore, our data suggest that prolonged ingestion of OVA by sensitized mice results in an improvement of the metabolic consequences caused by experimental food allergy.

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“…Allergenic immunotherapy induces shift in the cytokine profile from Th2 subpopulation (IL-4 and IL-5) towards Th1 subpopulation (IFN-gamma) (uermöSi et al, 2010). The most significant role in the development of oral tolerance is played by IL-10 and TGF-β (rollAnd et al, 2009).…”

Section: Resultsmentioning

confidence: 99%

“…Recently, a lot of attention has been focused on novel specific immunomodulatory therapies for food allergy, including oral immunotherapy (OIT) and sublingual immunotherapy (SLIT) (BlumcHen et al, 2010;Frew, 2010). Allergen-specific immunotherapy (ASIT) has been reported to modify different aspects of the immune system, inducing shift of allergy-promoting Th2 cells to Th1 cells, epitope-specific T-cell anergy, and allergen-specific regulatory T cells that suppress the responses of effector T cells (ArpS et al, 1998;uermöSi et al, 2010). …”

mentioning

confidence: 99%

Pea proteins immunotherapy in peanut allergic mice model

Szymkiewicz¹,

Chudzik-Kozłowska²

2014

Acta Alimentaria

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Mice (Balb/c), with peanut allergy induced, were subjected to desensitization therapy with the use of pea protein extract (PE) or isolated globulin fractions: legumin (PL) and vicilin (PV). B-and T-cell responses to peanut proteins were analysed by determination of the IgE, IgG1, and IgG2a antibody levels in plasma and the concentration of IL-4, IFN-gamma and IL-10 cytokines secreted by isolated splenocytes.Conducted studies have demonstrated that immunotherapy with proteins resulted in the decrease of total IgE and peanut-specific IgG1 levels and significantly enhanced synthesis of peanut-specific IgG2a in plasma (ELISA method) and at the cellular level (ELISPOT type B). A successful and effective immunotherapy is related to the shift in profile of lymphocytes from Th2 subpopulation towards Th1 subpopulation. In our studies significant increase in the activity of Th1 lymphocytes was observed in groups desensitized with pea protein extracts (PE) and pea legumin fraction (PL). In these groups, significant statistic decrease in IL-4 secreted and increase in IL-10 level were found.Desensitization method with the use of pea proteins being suggested in the presented studies can be an alternative method for specific immunotherapy for people, especially with strong allergic reaction to peanuts; however, this method needs further studies with mouse model. Keywords: peanut hypersensitivity, specific immunotherapy, cross-reactivity, pea proteins, animal modelPeanut allergy is one of the most serious disorders among the immediate hypersensitivity reactions and it appears to be a growing problem. The most common treatment of food allergy is exclusion of the component causing hypersensitivity from diet. However, in case of allergy to peanuts, this method is not suitable due to the possible occurrence of peanuts in foods, cosmetics and pharmaceutical products. Another problem is that traces of peanut allergens are sufficient to induce strong reaction (HouriHAne et al., 1997;BlumcHen et al., 2010). Mechanism of peanuts allergy is the subject of extended studies; however, there are still more questions than answers related to this aspect. Recent studies have proven that extracts from peanuts and nuts, contrary to milk or eggs, were able to activate complement system both in mice and people, which increased their ability to induce anaphylaxis (kHodoun et al., 2009). However, lack of definitive explanation of the mechanism of food hypersensitivity to peanuts limits therapeutic applications (THyAgArAjAn et al., 2010). Recently, a lot of attention has been focused on novel specific immunomodulatory therapies for food allergy, including oral immunotherapy (OIT) and sublingual immunotherapy (SLIT) (BlumcHen et al., 2010;Frew, 2010). Allergen-specific immunotherapy (ASIT) has been reported to modify different aspects of the immune system, inducing shift of allergy-promoting Th2 cells to Th1 cells, epitope-specific T-cell anergy, and allergen-specific regulatory T cells that suppress the responses of effector T cells (ArpS et al., 1998...

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Mechanisms of allergen-specific desensitization

Cited by 87 publications

References 38 publications

Fcγ Receptors Inhibit Mouse and Human Basophil Activation

Fcγ Receptors Inhibit Mouse and Human Basophil Activation

Prolonged ingestion of ovalbumin diet by sensitized mice improves the metabolic consequences induced by experimental food allergy

Pea proteins immunotherapy in peanut allergic mice model

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