Human CD4+CD25+ T cells derived from the majority of atopic donors are able to suppress TH1 and TH2 cytokine production

Bellinghausen, Iris; Klostermann, Bettina; Knop, Jürgen; Saloga, Joachim

doi:10.1067/mai.2003.1412

Cited by 181 publications

(148 citation statements)

References 25 publications

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“…With regards to Treg in allergic disorders, compelling evidence has been provided by Foxp3-deficient (scurfy) mice that reproduce the intense lymphoproliferation and allergic inflammation observed in patients with immune dysregulation polyendocrinopathy enteropathy-X-linked syndrome (41,42). Also relevant to allergic airway disease are results from clinical studies showing the ability of Treg to down-regulate Th2 cytokine production, albeit with an apparent inability to suppress the accompanying allergic airway inflammation (15,17). Conversely, two experimental studies using transgenic mice have suggested that Treg control allergic airway inflammation rather than AHR (13,43), although a recent study by Lewkowich et al (25) has indicated that Treg play a major role in the strain-specific protection of normal mice (adults) against both allergic airway inflammation and AHR.…”

Section: Discussionmentioning

confidence: 99%

“…Because Treg appear early in life and are extremely efficacious at restraining inflammatory responses, it has been suggested that Treg also participate in the control of allergic asthma by maintaining the tolerance to nonself Ags (13,14). In asthmatic patients, however, it is not clear whether Th2-skewed responses are favored by dysfunctional Treg or whether allergic inflammation overwhelms normally functioning Treg (15)(16)(17). To our knowledge, the mechanisms controlling the development of allergic airway disease in newborns have not yet been addressed.…”

Section: Targeting Of Cd25 and Glucocorticoid-induced Tnf Receptor Famentioning

confidence: 95%

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Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice

Hubeau¹,

Apostolou

Kobzik

2007

The Journal of Immunology

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Immunological mechanisms leading to increased asthma susceptibility in early life remain obscure. In this study, we examined the effects of neonatal Ab treatments targeting T cell populations on the development of an asthma syndrome. We used a model of increased asthma susceptibility where offspring of asthmatic BALB/c mother mice are more prone (than normal pups) to develop the disease. Neonatal pretreatment of naive pups with mAb directed against the IL-2Rα chain (CD25), the costimulatory molecule glucocorticoid-induced TNFR family related gene, and the inhibitory molecule CTLA-4 elicited contrasting effects in offspring depending on the mother’s asthma status. Specifically, neonatal CD25high T cell depletion stimulated asthma susceptibility in normal offspring whereas it ameliorated the condition of pups born of asthmatic mothers. Conversely, glucocorticoid-induced TNFR family related gene ligation as a primary signal reduced the spleen cellularity and largely abrogated asthma susceptibility in asthma-prone offspring, without inducing disease in normal pups. Striking changes in Th1/Th2 cytokine levels, especially IL-4, followed mAb pretreatment and were consistent with the impact on asthma susceptibility. These results point to major differences in neonatal T cell population and responsiveness related to maternal asthma history. Interventions that temporarily remove and/or inactivate specific T cell subsets may therefore prove useful to attenuate early life asthma susceptibility and prevent the development of Th2-driven allergic airway disease.

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Section: Discussionmentioning

confidence: 99%

Section: Targeting Of Cd25 and Glucocorticoid-induced Tnf Receptor Famentioning

confidence: 95%

Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice

Hubeau¹,

Apostolou

Kobzik

2007

The Journal of Immunology

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“…Treg may block the transition from the early activation stage to the differentiated T helper 2 (Th2) state, limit airway allergic inflammation and act to prevent inappropriate Th2 responses to environmental allergens [15,16]. Several independent lines of evidence indicate that the number or function of Treg is impaired or altered in patients with allergies compared with healthy individuals [17][18][19][20][21][22]. However, data concerning the role of Treg in the pathogenesis of paediatric allergic disease are rare.…”

Section: Cd25mentioning

confidence: 99%

“…It also impairs the activation of mast cells and eosinophils and promotes the synthesis of IgG4 [34]. Resolution of allergen-induced airway inflammation and hyperreactivity related to the transfer of allergen-specific Treg cells in vivo depends on the Bellinghausen [21] n.a.…”

Section: Cd25mentioning

confidence: 99%

The levels of CD4+CD25+ regulatory T cells in paediatric patients with allergic rhinitis and bronchial asthma

Lee

Wang

et al. 2007

Clinical and Experimental Immunology

169

109

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SummaryOur purpose was to determine whether numbers of CD4 + CD25 + T [T regulatory (Treg)] cells and mRNA expression of functional molecules of Treg are related to airway allergy and disease severity in 51 paediatric patients with allergic rhinitis or bronchial asthma and 47 healthy controls. Surface markers were evaluated with flow cytometry, and mRNA was determined with realtime polymerase chain reaction. Children with allergic disease had fewer CD4 + CD25 + T cells (8·49% Ϯ 2·41% versus 9·58% Ϯ 2·43%, P < 0·05) and CD4 + CD25 hi T cells (1·32% Ϯ 0·68% versus 1·70% Ϯ 0·68%, P < 0·01) than control subjects. Numbers of CD4 + CD25 + and CD4 + CD25 hi T lymphocytes were higher in children with persistent allergic rhinitis and/or moderatesevere bronchial asthma than in those with respective milder disease. The number of Treg cells was correlated positively with total immunoglobulin E level. The mRNA expression of forkhead box P3 (FoxP3) was increased in moderate-severe versus mild asthma (2·93 Ϯ 0·38 versus 1·60 Ϯ 0·31, P < 0·01). Patients with moderate-severe bronchial asthma also had increased mRNA expression of interleukin (IL)-10 compared with patients with mild asthma (15·24 Ϯ 4·07 versus 3·77 Ϯ 2·18, P < 0·01). The suppressive function of Treg cells from patients with more severe asthma was competent in vitro. On average, decreased numbers of Treg cells in children with allergic airway disease might represent a defect of the Treg population. With increased expression of FoxP3 and IL-10 in Treg from patients with relatively severe allergic disease, adaptive and functional Treg might be generated in response to aggravated atopy and disease severity.

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“…16) These nTreg cells produce both IL-10 and TGF-β and are known to suppress inflammation in both normal and allergic conditions. 17) Here, we examined the influence of L-92 on nTreg cells to clarify the immunomodulatory capacity by suppressing ACD in mice.…”

Section: Cd25mentioning

confidence: 99%

Lactobacillus acidophilus Strain L-92 Induces CD4+CD25+Foxp3+ Regulatory T Cells and Suppresses Allergic Contact Dermatitis

Shah

Saio

Yamashita

et al. 2012

Biological & Pharmaceutical Bulletin

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The anti-allergic mechanism of heat-killed Lactobacillus acidophilus strain L-92 has not been fully investigated. Recent studies have reported that CD4 CD25 Foxp3 (forkhead box P3) T regulatory (Treg) cells play important roles in controlling allergic diseases. Hence, we examined the effect of orally administered L-92 on CD4 CD25 Foxp3 cell populations. BALB/c mice were supplemented daily with L-92 by gavage for 5 weeks. 2,4-Dinitrofluorobenzene (DNFB) was used to induce allergic contact dermatitis (ACD) in mice. Fluorescent-activated cell sorter (FACS) analysis was used to determine CD4 CD25 Foxp3 T cell populations in spleen and cervical lymph nodes (CLN). Interleukin-10 (IL-10), transforming growth factor-β (TGF-β), and Foxp3 mRNA expressions in mouse ear skin were investigated by real-time reverse transcription-polymerase chain reaction (RT-PCR). The percentage of CD4 CD25 Foxp3 T cell populations were significantly increased in both spleen and CLN of L-92-fed group than vehicle and control. In addition, L-92 produced higher levels of Foxp3, IL-10 and TGF-β compared to control mice. These results suggest that L-92 can up-regulate the number of Treg cells to suppress the progression of DNFB-induced contact dermatitis in mice. Key words contact dermatitis; Lactobacillus acidophilus strain L-92; regulatory T cell; forkhead box P3Commensal bacteria of the gut flora affect host physiology through diverse mechanisms, including modulation of the host immune system and attenuation of gastrointestinal (GI) diseases. Some clinical and experimental animal studies reported that certain commensal bacteria may also be able to regulate immune responses outside of the GI tract. Among them, species of lactobacilli and bifidobacteria are prominent commensal bacteria with anti-allergic properties. For example, a double-blind placebo-control study, Lactobacillus (L.) rhamnosus GG 1) and L. fermentum VRI-003 PCC 2) reduced the development of eczema in young children. Within the experimental allergy animal models, several lactic acid bacterial (LAB) strains, including L. casei strain Shirota, 3) and L. brevis strain SBC8803 4) inhibits antigen specific immunoglobulin E (IgE) production, and L. paracasei strain KW3110 5) was found to suppress atopic dermatitis (AD)-like skin lesions. We also previously demonstrated that heat-killed L. acidophilus strain L-92 (L-92) can suppress both 2,4-dinitrofluorobenzene (DNFB) and mite antigen-induced AD-like skin lesions in mice.6) Despite some pre-clinical studies on animal models as well as clinical trials have highlighted the beneficial roles of these bacteria, the exact mechanisms behind the anti-allergic effects still remain obscure.Allergic contact dermatitis (ACD) is a delayed-type hypersensitivity caused by an allergic reaction to some chemical (hapten) in contact with the skin. The allergic condition causes itching and inflammation of the skin manifested by varying degrees of erythema, edema, and vesiculation. Knowledge of the mechanism of ACD was derived mainly from animal models in...

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Human CD4+CD25+ T cells derived from the majority of atopic donors are able to suppress TH1 and TH2 cytokine production

Cited by 181 publications

References 25 publications

Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice

Targeting of CD25 and Glucocorticoid-Induced TNF Receptor Family-Related Gene-Expressing T Cells Differentially Modulates Asthma Risk in Offspring of Asthmatic and Normal Mother Mice

The levels of CD4+CD25+ regulatory T cells in paediatric patients with allergic rhinitis and bronchial asthma

<i>Lactobacillus acidophilus</i> Strain L-92 Induces CD4<sup>+</sup>CD25<sup>+</sup>Foxp3<sup>+</sup> Regulatory T Cells and Suppresses Allergic Contact Dermatitis

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