Atopic disorders: a default pathway in the absence of infection?

Erb, Klaus J.

doi:10.1016/s0167-5699(99)01475-9

Cited by 81 publications

(51 citation statements)

References 51 publications

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“…The orientation of naive T cells toward a Th1 profile could result from the induction of transcription factors responsible for the global generation of Th1 cells and/or from the suppression of transcription factors needed for the differentiation of Th2 cells as has been hypothesized by Erb (37).…”

Section: Discussionmentioning

confidence: 97%

Bordetella pertussisInfection in 2-Month-Old Infants Promotes Type 1 T Cell Responses

Mascart

Verscheure

Malfroot

et al. 2003

The Journal of Immunology

125

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Neonatal immaturity of the immune system is currently believed to generally limit the induction of immune responses to vaccine Ags and to skew them toward type 2 responses. We demonstrated here that Bordetella pertussis infection in very young infants (median, 2 mo old) as well as the first administration of whole-cell pertussis vaccine induces B. pertussis Ag-specific IFN-γ secretion by the PBMC of these infants. IFN-γ was secreted by both CD4+ and CD8+ T lymphocytes, and the levels of Ag-induced IFN-γ secretion did not correlate with the age of the infants. Appearance of the specific Th-1 cell-mediated immunity was accompanied by a general shift of the cytokine secretion profile of these infants toward a stronger Th1 profile, as evidenced by the response to a polyclonal stimulation. We conclude that the immune system of 2-mo-old infants is developmentally mature enough to develop Th1 responses in vivo upon infection by B. pertussis or vaccination with whole-cell pertussis vaccines.

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Section: Discussionmentioning

confidence: 97%

Bordetella pertussisInfection in 2-Month-Old Infants Promotes Type 1 T Cell Responses

Mascart

Verscheure

Malfroot

et al. 2003

The Journal of Immunology

125

View full text Add to dashboard Cite

show abstract

“…Consequently, it is not surprising that there are many possible modalities to treat the ailment (2-7). Since the identification of distinct Th cell subsets that differ in cytokine production and effector functions as they relate to allergic asthma, a challenging concept has evolved to allow the use of therapeutic modalities that will modulate Th1/Th2 balance in asthma without deleterious side effects (8,9). Primarily, these concepts have focused on modulation of Ag presentation to T cells and inhibition of Ag-specific Th2 responses and/or increasing the Th1 response (10).…”

Section: Flt-3 Ligand Reverses Late Allergic Response and Airwaymentioning

confidence: 99%

Flt-3 Ligand Reverses Late Allergic Response and Airway Hyper-Responsiveness in a Mouse Model of Allergic Inflammation

Edwan

Perry²,

Talmadge

et al. 2004

The Journal of Immunology

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Flt3 ligand (Flt3-L) is a growth factor for dendritic cells and induces type 1 T cell responses. We recently reported that Flt3-L prevented OVA-induced allergic airway inflammation and suppressed late allergic response and airway hyper-responsiveness (AHR). In the present study we examined whether Flt3-L reversed allergic airway inflammation in an established model of asthma. BALB/c mice were sensitized and challenged with OVA, and AHR to methacholine was established. Then mice with AHR were randomized and treated with PBS or 6 μg of Flt3-L i.p. for 10 days. Pulmonary functions and AHR to methacholine were examined after rechallenge with OVA. Treatment with Flt3-L of presensitized mice significantly suppressed (p < 0.001) the late allergic response, AHR, bronchoalveolar lavage fluid total cellularity, absolute eosinophil counts, and inflammation in the lung tissue. There was a significant decrease in proinflammatory cytokines (TNF-α, IL-4, and IL-5) in bronchoalveolar lavage fluid, with a significant increase in serum IL-12 and a decrease in serum IL-5 levels. There was no significant effect of Flt3-L treatment on serum IL-4 and serum total IgE levels. Sensitization with OVA significantly increased CD11b+CD11c+ cells in the lung, and this phenomenon was not significantly affected by Flt3-L treatment. These data suggest that Flt3-L can reverse allergic airway inflammation and associated changes in pulmonary functions in murine asthma model.

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“…The 'hygiene hypothesis' suggests that exposure to microbial infections or microbial products may inhibit the development or pathogenesis of allergic responses, including asthma. [1][2][3][4][5] Many epidemiological observations related to various infections support this provocative hypothesis. [6][7][8][9][10][11][12][13][14] In particular, a series of studies have described children who had close contact with farm animals and exhibited significantly lower levels of allergy and asthma later in life.…”

Section: Introductionmentioning

confidence: 99%

Role of dendritic cells: a step forward for the hygiene hypothesis

Yang

Gao

2010

Cell Mol Immunol

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The hygiene hypothesis was proposed more than two decades ago, but its mechanism remains unclear. This review focuses on recent advances in the field, especially on the role played by dendritic cells (DCs) and their modulating effects on various infections and allergic diseases, including allergic asthma. DCs isolated from mice long after the resolution of an infection were reported to have a significant modulating effect on allergen-specific Th2 responses in both in vitro and in vivo systems. These DCs showed DC1-like and/or tolerogenic DC capacity, which allowed for the inhibition of allergic responses by immune deviation (enhancing Th1 response) and immune regulation (through regulatory T-cell and Th2 hyporesponsiveness) mechanisms. These findings represented a significant advance in the elucidation of the mechanisms underlying the hygiene hypothesis. Further investigation on the mechanisms by which DCs are 'educated' by infectious agents and the influence of the type, time, and extent of infections on this 'education' process will help us understand immune regulation in disease settings and in the rational design of preventive/therapeutic approaches to allergy/asthma and infections.

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Atopic disorders: a default pathway in the absence of infection?

Cited by 81 publications

References 51 publications

Bordetella pertussisInfection in 2-Month-Old Infants Promotes Type 1 T Cell Responses

Bordetella pertussisInfection in 2-Month-Old Infants Promotes Type 1 T Cell Responses

Flt-3 Ligand Reverses Late Allergic Response and Airway Hyper-Responsiveness in a Mouse Model of Allergic Inflammation

Role of dendritic cells: a step forward for the hygiene hypothesis

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