Numerical and Functional Deficiency of Suppressor T Cells Precedes Development of Atopic Eczema

Chandra, R. K.; Baker, Maryanne

doi:10.1016/s0140-6736(83)90924-8

Cited by 67 publications

(20 citation statements)

References 12 publications

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“…The underlying mech anism is not known but several observations indicate that a primary defect in the suppression of the IgE an tibody formation [4] may be responsible for this. Thus, several abnormalities in T lymphocytes have been described in clinically healthy infants who later develop allergic disease, including low numbers of T cells rosetting with sheep erythrocytes [5], low num bers of T cells with the surface marker OKTs which is associated with suppressor cell activity and low Con A-driven suppression [6].…”

Section: Introductionmentioning

confidence: 99%

Intrauterine Exposure to the Beta-Adrenergic Receptor-Blocking Agent Metoprolol and Allergy

Björkstén

Finnström²,

Wichman³

1988

Int Arch Allergy Immunol

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Cord blood IgE levels and the development of allergy were studied in 29 children born by mothers who had been treated with the β-adrenergic receptor blocking agent, metoprolol, during the pregnancy and in 23 children of placebo-treated mothers. In 13 (45%) of the former and 3 (15%) of the placebo group elevated cord blood IgE levels, i.e. more than 0.9 kU/l and/or obvious or probable allergy developed (p = 0.03). The findings support previous experimental observations that β-blocking agents may enhance IgE antibody formation. It also adds to the number of environmental factors that may increase the risk for atopic disease in children.

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Section: Introductionmentioning

confidence: 99%

Intrauterine Exposure to the Beta-Adrenergic Receptor-Blocking Agent Metoprolol and Allergy

Björkstén

Finnström²,

Wichman³

1988

Int Arch Allergy Immunol

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“…In fact, a reduced percentage of T cells or of positive T8 lymphocytes was found in patients with atopic dermatitis and in those with E-hypergammaglobulin emia [Romagnani et al, 1978;Canonica et al, 1979;Faure et al, 1982;Leung et al, 1983;Chandra and Baker, 1983], A de pressed lymphoproliférative response to T-cell mitogens was also demonstrated [Grove et al, 1975;Rivlin et al, 1981;Romagnani et al, 1985].…”

Section: Discussionmentioning

confidence: 99%

“…Deficiency in T cells was more pronounced in certain subsets of T lym phocytes. In fact, no significant modifica tion of helper responsiveness has been found, while many data suggest the pres ence of a relative, selective suppressor Tcell deficiency in atopic patients with high serum levels of immunoglobulin E [Canonica et al, 1979;Bruno et al, 1983;Faure et al, 1982;Chandra and Baker, 1983;Kesarwala et al, 1984], Moreover, a signi ficant reduction in NK-cell activity has been shown in patients with atopic derma titis [Lever et al, 1984], Obviously, defects in the host defense system may predispose to greater than normal susceptibility to bacterial, viral and mycotic infections [Rosen et al, 1984], Conflicting results have been reported about the susceptibility of atopic patients to infections. It is well known that patients with severe atopic dermatitis [Jones et al, 1973;Hanifin and Lobitz, 1977;Minor et al, 1974] and atopic children less than 1 year of age frequently suffer from serious and recurrent infections.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the Host Defense System in Asthmatic Patients

et al. 1986

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The efficiency of some components of the host defense system has been evaluated in 32 atopic patients with rhinitis, asthma or asthma and rhinitis. No alterations in components of complement (C3 and C4), serum immunoglobulins (IgG, IgA, and IgM) and neutrophil functional parameters were found. As expected, serum IgE values were higher than in controls. A decreased percentage of total circulating T lymphocytes, an increased percentage of la 1-positive cells, but normal values of OKT4- and OKT8-positive T lymphocytes were demonstrated. However, a greater heterogeneity in the distribution of the suppressor-cytotoxic subset was shown in atopic patients.

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“…(e) Patients with atopic dermatitis and those with E-hypergammaglobulinemia have in creased percentages of T4+ and reduced percentages of T8+ lymphocytes [16,17]. (f) The defect of T-cell subsets precedes clinical atopic disease and seems to be of primary pathogenetic importance, as well as of predictive value [18]. (g) Atopies seem to have a decreased phenotypic ex pression of T cell H-2 receptors and pro duce fewer suppressor signals than T cells from nonatopics.…”

Section: Impairment O F Ige-specific Regulatory Tcells In Atopic Subjmentioning

confidence: 99%

New Trends on the Pathogenetic Aspects of Allergic Bronchial Asthma

Prete¹,

Maggi²,

Romagnani³

1986

Respiration

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The central role of IgE antibodies in allergic bronchial asthma (ABA) is not disputed any longer. Immunological mechanisms other than IgE-mediated reactions in the pathogenesis of ABA have not yet been definitely demonstrated. There is controversy as to whether IgG STS antibodies, probably IgG4, play a role in the disease process. There is no evidence to support the involvement of immune complexes. Anti-beta-2-adrenergic receptor autoimmune responses cannot be considered as responsible for the development of the disease at the present time. In the last few years a great effort has been made to understand the immunological mechanisms underlying the enhanced and long-standing IgE antibody production in atopic diseases. The results obtained in different laboratories, including our own, are in favor of a high responder status to allergen epitopes in a large proportion of atopies and suggest that a preferential expression of IgE isotype in the antibody responses may occur through different mechanisms. Of great interest is the recent demonstration of IgE-binding factors with IgE-potentiating and suppressive activity and of other related regulatory molecules and receptors. Progress has been recently achieved in the characterization of mediators responsible for the different pathological changes of ABA. A linkage between immediate IgE-mediated reactions, bronchial late-phase reactions (LPR) and chronic inflammation (CI) has been reported. It has been demonstrated that a cascade of mediators and cell interactions induce both LPR and CI. There is evidence of a close relationship between LPR-CI and nonspecific bronchial hyperreactivity. A better knowledge of pathogenetic mechanisms of ABA would open new perspectives in the therapy. A modulation of IgE antibody production can be attempted in different ways. At present a control of mediator release and of airway hyperreactivity can be achieved by several pharmacological interventions and by the avoidance of common and/or occupational allergens or pollutants.

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Numerical and Functional Deficiency of Suppressor T Cells Precedes Development of Atopic Eczema

Cited by 67 publications

References 12 publications

Intrauterine Exposure to the Beta-Adrenergic Receptor-Blocking Agent Metoprolol and Allergy

Intrauterine Exposure to the Beta-Adrenergic Receptor-Blocking Agent Metoprolol and Allergy

Evaluation of the Host Defense System in Asthmatic Patients

New Trends on the Pathogenetic Aspects of Allergic Bronchial Asthma

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