Role of regulatory T cells in allergy and asthma

Akbari, Omid; Stock, Philippe; DeKruyff, Rosemarie H.; Umetsu, Dale T.

doi:10.1016/j.coi.2003.09.012

Cited by 176 publications

(132 citation statements)

References 75 publications

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“…A possible explanation for our findings may be that antenatal infections or inflammation associated with chorioamnionitis could modulate lung development and injury (40). Alternatively, as discussed by other investigators, antibiotics can cross the placenta and enter the fetal circulation or can modify maternal microbial load during pregnancy (7), and have an effect on infant gut colonization and hence on the maturation and differentiation of the mucosal immune system (41,42). This may also explain the small increase in risk of early-onset wheezing we found in children of mothers who received antibiotics at delivery.…”

Section: Discussionmentioning

confidence: 71%

Maternal Complications and Procedures in Pregnancy and at Birth and Wheezing Phenotypes in Children

Rusconi

Galassi

Forastiére

et al. 2007

Am J Respir Crit Care Med

136

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Rationale: There is increasing interest in the potential influence of fetal and early life conditions on childhood wheezing. Objectives: To investigate the associations between maternal complications and procedures in pregnancy and at birth and the risk of various wheezing phenotypes in young children. Methods: We studied 15,609 children, aged 6-7 yr, enrolled in a population-based study. Standardized questionnaires were completed by the children's mothers. AT A GLANCE COMMENTARY Scientific Knowledge on the SubjectMaternal smoking in pregnancy influences lung development and is associated with wheezing in childhood; other prenatal and perinatal factors (maternal infections, obstetric conditions) have been inconclusively associated with wheezing among offspring. What This Study Adds to the FieldAn association was found between maternal hypertension, diabetes, and urinary tract infections during pregnancy and exposure to antibiotics at delivery with wheezing disorders, in particular wheezing of early onset.(1). The most studied in utero environmental influence on lung development is maternal smoking in pregnancy, which has been shown to be associated not only with wheezing in childhood (2-5) but also with a dose-related reduction in lung function in the newborn period. Fetal development seems therefore to represent a critical time of pulmonary vulnerability with respect to smoking exposure. More recently, some studies have also investigated the relationships between exposure to maternal infections in pregnancy (6-8), maternal obstetric conditions (hyperemesis, hypertension, and preeclampsia) (9-11), uterine factors (antepartum hemorrhage, preterm contractions, placental insufficiency, and uterine growth restriction) (9-11), malposition or malpresentation of the fetus (11), mode of delivery (11)(12)(13)(14)(15)(16)(17)(18), and the development of asthma among offspring. However, the findings of these studies have been inconsistent.In a report published in 1999 (19), we found associations between a number of pre-, peri-, and early postnatal factors and different wheezing phenotypes in a large multicenter crosssectional population-based study, the SIDRIA (Italian Studies of Respiratory Disorders in Childhood and the Environment) phase 1 study, an extension of the International Study on Asthma and Allergies in Childhood (ISAAC) phase 1 study (20). The enrolled children were categorized, on the basis of criteria derived from Martinez and coworkers (21), as transient early wheezers (children with wheezing in the first 2 yr of life but not at school age), persistent wheezers (children who continued to wheeze at school age), late-onset wheezers (children who did not wheeze in the first years of life but who wheezed when 6-7 yr

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Section: Discussionmentioning

confidence: 71%

Maternal Complications and Procedures in Pregnancy and at Birth and Wheezing Phenotypes in Children

Rusconi

Galassi

Forastiére

et al. 2007

Am J Respir Crit Care Med

136

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“…T reg cells mediate peripheral tolerance towards allergens and autoantigens in a cell contact and/or cytokine-dependent manner [7] and are characterized by the expression of CD25, CD62L or CD103, the suppressive cytokines IL-10 and transforming growth factor-b 1 (TGFb 1 ) and the key transcription factor FOXP3 [8]. Because T reg cells are crucial in mediating tolerance towards allergens, novel treatment strategies are aiming on the generation of these cells [9].…”

Section: Introductionmentioning

confidence: 99%

High‐Altitude Climate Therapy Reduces Local Airway Inflammation and Modulates Lymphocyte Activation

Karagiannidis¹,

Hense

Rueckert³

et al. 2006

Scand J Immunol

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High-altitude climate therapy is a well-established therapeutic option, which improves clinical symptoms in asthma. However, little is known about the underlying immunological mechanisms. The study investigates the influence of high-altitude climate therapy on airway inflammation and cellular components of specific and unspecific immune response. Exhaled NO significantly decreased within 3 weeks of therapy in patients with allergic and intrinsic, moderate and severe asthma. Interleukin-10 (IL-10)-secreting peripheral blood mononuclear cells (PBMC) increased within 3 weeks of therapy in six of 11 patients, whereas transforming growth factor-b 1 -secreting PBMC remained stable. Furthermore, monocyte activation, assessed by CD80 expression significantly decreased during therapy. The frequency of CRTH2-expressing T cells decreased, while regulatory T cells (T reg ) remained stable. FOXP3 and GATA-3 mRNA expression in CD4 þ T cells did not change, while interferon-g and IL-13 mRNA expression decreased in eight of 10 patients. The current data demonstrate that high-altitude climate therapy reduces local airway inflammation. Furthermore, monocytes switch towards a tolerogenic phenotype under high-altitude climate therapy. The T reg /Th2 ratio increases; however, because of the absence of antigens/allergens, no de novo differentiation of Th2 nor T reg cells is observed. The high-altitude climate therapy therefore may form the immunological basis for the endogenous control of allergen-driven diseases.

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“…Other cytokines, such as tumor necrosis factor (TNF), have been demonstrated to amplify the effect of asthmatic inflammation (29,42). Recently, a role of regulatory T cells (Th3 cells, T R cells, CD4 ϩ CD25 ϩ cells, and natural killer T cells) has been suggested in the control of asthma and allergy, but the specific mechanisms are still unknown (2).…”

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confidence: 99%

Antigen sensitization modulates alveolar macrophage functions in an asthma model

Careau¹,

Proulx²,

Pouliot³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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-We have previously demonstrated that adoptive transfer of alveolar macrophages from allergy-resistant rats to alveolar macrophage-depleted allergic rats prevents airway hyperresponsiveness development, suggesting an important role for alveolar macrophages in asthma pathogenesis. Given that ovalbumin sensitization can modulate alveolar macrophage cytokine production, we investigated the role of sensitized and unsensitized alveolar macrophages in an asthma model. Alveolar macrophages from unsensitized or sensitized Brown Norway rats were transferred to alveolar macrophage-depleted sensitized rats 24 h before allergen challenge. Airway responsiveness to methacholine and airway inflammation were measured the following day. Methacholine concentration needed to increase lung resistance by 200% was significantly higher in alveolar macrophage-depleted sensitized rats that received unsensitized alveolar macrophages compared with alveolar macrophage-depleted sensitized rats that received sensitized alveolar macrophages. Tumor necrosis factor levels in bronchoalveolar lavage fluid of sensitized rats that received unsensitized alveolar macrophages were significantly lower compared with rats that received sensitized alveolar macrophages. Interestingly, alveolar macrophages of unsensitized animals showed higher phagocytosis activity compared with alveolar macrophages of sensitized rats, suggesting that sensitization modulates alveolar macrophage phagocytosis function. Our data suggest an important role of allergen sensitization on alveolar macrophage function in asthma pathogenesis. airway hyperresponsiveness; cytokine; phagocytosis THE INCIDENCE OF allergic respiratory diseases increased dramatically over the last two decades. The genetic predisposition to develop asthma is now well recognized (20). Numerous studies have also shown the importance of inflammatory cells, such as mast cells, lymphocytes, eosinophils, and neutrophils, as well as Th2 type cytokines in asthma (6,19,32). Interleukin (IL)-4 and IL-13, two Th2 cytokines, are important in immunoglobulin (Ig) class switching to IgE, whereas IL-4 and IL-10 play a crucial role in Th2 cell commitment (9,16,50). In contrast, Th1 cytokines (interferon-␥ and IL-12) protect against asthma development in children (48). Other cytokines, such as tumor necrosis factor (TNF), have been demonstrated to amplify the effect of asthmatic inflammation (29,42). Recently, a role of regulatory T cells (Th3 cells, T R cells, CD4 ϩ CD25 ϩ cells, and natural killer T cells) has been suggested in the control of asthma and allergy, but the specific mechanisms are still unknown (2).Alveolar macrophages (AM) are predominant immune effector cells in the alveolar spaces and conducting airways and play a key role in the immunological homeostasis of the lung (8, 30, 43). Although they are well known to suppress T cell activation and antigen presentation activities of dendritic cells (22,41), their role in asthma is still debated. Using the liposome-mediated macrophage suicide technique (47), we have...

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Role of regulatory T cells in allergy and asthma

Cited by 176 publications

References 75 publications

Maternal Complications and Procedures in Pregnancy and at Birth and Wheezing Phenotypes in Children

Maternal Complications and Procedures in Pregnancy and at Birth and Wheezing Phenotypes in Children

High‐Altitude Climate Therapy Reduces Local Airway Inflammation and Modulates Lymphocyte Activation

Antigen sensitization modulates alveolar macrophage functions in an asthma model

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