Long-term anergy in orally tolerized mice is linked to decreased B7.2 expression on B cells

Futata, E.; Brito, Cyro Alves de; Victor, Jefferson Russo; Fusaro, Ana Elisa; Oliveira, C. R.; Maciel, Milton; Duarte, Alberto José da Silva; Sato, Maria Notomi

doi:10.1016/j.imbio.2005.08.006

Cited by 17 publications

(19 citation statements)

References 36 publications

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“…The offspring of mothers subjected to low allergen exposure during pregnancy developed a state of immunological unresponsiveness, reflected by the inhibition of the antigen‐proliferative response and minimal Th1/Th2 cytokine production, as well as the inhibition of total IgE levels and specific IgG1 and IgG2a antibody levels. The effect of oral tolerance induction followed by mucosal administration of allergens or food antigens in adult mice is well known 28–32 . One of the regulatory mechanism mediated in oral tolerance has been showed to be exerted by TGF‐β 1 , 31 in the prevention of allergy 29 and in airway remodelling.…”

Section: Discussionmentioning

confidence: 99%

“…The effect of oral tolerance induction followed by mucosal administration of allergens or food antigens in adult mice is well known. [28][29][30][31][32] One of the regulatory mechanism mediated in oral tolerance has been showed to be exerted by TGF-b 1 , 31 in the prevention of allergy 29 and in airway remodelling. Exposure of lactating mice to OVA may cause the transfer of antigen to their progeny through breast milk, resulting in antigen-specific tolerance and prevention of allergen-induced lung pathology.…”

Section: Discussionmentioning

confidence: 99%

“…The ELISA for transforming growth factor‐β 1 (TGF‐β 1 ; Promega, Madison, WI) in milk samples was performed following the manufacturer’s recommendations. Interleukin‐4 (IL‐4), IL‐10 and interferon‐γ (IFN‐γ; OPTEiaTM PharMingen) were measured in supernatants of spleen cell cultures with anti‐CD3 monoclonal antibody (2 μg/ml; PharMingen) for 24 hr or OVA (200 μg/ml; Sigma) and HEL (200 μg/ml; Sigma) for 72 hr, as previously described 28 whereupon cell‐free supernatants were stored at −70° until the cytokine assay by means of ELISA. Detection limits of IL‐4, IL‐10, IFN‐γ and TGF‐β 1 were 3·9, 31·2, 15·6 and 32 pg/ml, respectively.…”

Section: Methodsmentioning

confidence: 99%

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Balance between early life tolerance and sensitization in allergy: dependence on the timing and intensity of prenatal and postnatal allergen exposure of the mother

et al. 2009

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Balance between early life tolerance and sensitization in allergy: dependence on the timing and intensity of prenatal and postnatal allergen exposure of the mother Introduction Early childhood is a phase of life with a high risk of allergic sensitization -it is the time when initial allergen sensitization frequently occurs.1,2 The immature status of the immune system in early life, 3,4 and the predisposition towards T helper type 2 (Th2) skewing of immune function during fetal and neonatal periods 5,6 may collectively contribute to the initial development of an allergic response subsequent to allergen exposure. Maternal allergen exposure seems to be a risk factor for early atopic disorders, influenced by genetic and environmental factors. 7,8 Therefore, it is important to understand the relationship between the amount and timing of initial allergen exposure as a factor in the early development of sensitization.Maternally derived dietary allergen exposure has been associated with the presence of the allergen in fetal circulation, implying that the fetus may be exposed to dietary allergen during pregnancy transplacentally or SummaryAllergens can be maternally transferred to the fetus or neonate, though it is uncertain how this initial allergen exposure may impact the development of allergy responses. To evaluate the roles of timing and level of maternal allergen exposure in the early life sensitization of progeny, female BALB/c mice were given ovalbumin (OVA) orally during pregnancy, lactation or weekly at each stage to investigate the immunoglobulin E (IgE) antibody production and cellular responsiveness of their offspring. Exposure to OVA during pregnancy was also evaluated in OVA-specific T-cell receptor (TCR) transgenic (DO11.10) mice. The effect of prenatal antigen exposure on offspring sensitization was dependent on antigen intake, with low-dose OVA inducing tolerance followed by neonatal immunization that was sustained even when pups were immunized when 3 weeks old. These offspring received high levels of transforming growth factor-b via breastfeeding. High-dose exposure during the first week of pregnancy or perinatal period induced transient inhibition of IgE production following neonatal immunization; although for later immunization IgE production was enhanced in these offspring. Postnatal maternal antigen exposure provided OVA transference via breastfeeding, which consequently induced increased offspring susceptibility to IgE antibody production according to week post-birth. The effect of low-dose maternal exposure during pregnancy was further evaluated using OVA transgenic TCR dams as a model. These progeny presented pronounced entry of CD4 + T cells into the S phase of the cell cycle with a skewed T helper type 2 response early in life, revealing the occurrence of allergen priming in utero. The balance between tolerance and sensitization depended on the amount and timing of maternal allergen intake during pregnancy.Keywords: breastfeeding; immunoglobulin E antibodies; in utero priming; maternal allerg...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Balance between early life tolerance and sensitization in allergy: dependence on the timing and intensity of prenatal and postnatal allergen exposure of the mother

et al. 2009

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“…Long-term anergy to food protein in orally tolerised mice is linked to decreased CD86 expression on B cells, favouring a Th1 shift [34]. It is presently unclear whether the same or different co-stimulatory pathways are necessary for oral tolerance to chemicals.…”

Section: Haptensmentioning

confidence: 99%

Does hapten exposure predispose to atopic disease? The hapten-atopy hypothesis

McFadden

White

Basketter

et al. 2009

Trends in Immunology

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“…Our group has been investigating adoptive maternal-foetal immune interactions in the context of allergy regulation. [1][2][3][4][5][6][7][8][9][10] The potential of IgG antibodies as allergy regulators has been discussed for decades. In the early 80s, direct evidence that maternal IgG can suppress IgE production in offspring was obtained in a murine model of ovalbumin (OVA) immunization.…”

Section: Introductionmentioning

confidence: 99%

Low doses of IgG from atopic individuals can modulatein vitroIFN-γ production by human intra-thymic TCD4 and TCD8 cells: An IVIg comparative approach

Sgnotto

Oliveira

Lira

et al. 2017

Human Vaccines & Immunotherapeutics

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The regulatory effect of allergic responses induced by IgG antibodies on human intra-thymic cells has not been reported in the literature. The aim of this study was to evaluate the possible differential effect of purified IgG from atopic and non-atopic individuals on human intra-thymic αβT cell cytokine production. Thymic tissues were obtained from 14 patients who were less than 7 d old. Additionally, blood samples were collected from atopic and non-atopic volunteers. Thymocytes and peripheral blood mononuclear cells were cultured with purified atopic or non-atopic IgG, and intracellular cytokine production was assessed. Purified IgG did not influence the frequency or viability of human intra-thymic αβT cells. Purified non-atopic IgG induced greater IFN-γ production by intra-thymic CD4+CD8+ T cells than did the mock treatment and atopic IgG. A similar effect of purified non-atopic IgG on TCD8 cells was observed compared with the mock treatment. Atopic IgG inhibited IFN-γ and TGF-β production by intra-thymic TCD4 cells. Treatment with intravenous immunoglobulin resulted in intermediate levels of IFN-γ and TGF-β in intra-thymic TCD4 cells compared with treatment with atopic and non-atopic IgG. Peripheral TCD4 cells from non-atopic individuals produced IFN-γ only in response to atopic IgG. This report describes novel evidence revealing that IgG from atopic individuals may influence intracellular IFN-γ production by intra-thymic αβT cells in a manner that may favor allergy development.

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Long-term anergy in orally tolerized mice is linked to decreased B7.2 expression on B cells

Cited by 17 publications

References 36 publications

Balance between early life tolerance and sensitization in allergy: dependence on the timing and intensity of prenatal and postnatal allergen exposure of the mother

Balance between early life tolerance and sensitization in allergy: dependence on the timing and intensity of prenatal and postnatal allergen exposure of the mother

Does hapten exposure predispose to atopic disease? The hapten-atopy hypothesis

Low doses of IgG from atopic individuals can modulatein vitroIFN-γ production by human intra-thymic TCD4 and TCD8 cells: An IVIg comparative approach

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