Decreased production of IFN<sub>γ</sub> and increased production of IL‐6 by cord blood mononuclear cells of newborns with a high risk of allergy

Liao, Su-Wei; Liao, Tung-Nan; Chiang, Bor‐Luen; Huang, Maosheng; CHEN, C. C.; Chou, Chin Cheng; Hsieh, Kue‐Hsiung

doi:10.1111/j.1365-2222.1996.tb00555.x

Cited by 112 publications

(64 citation statements)

References 40 publications

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“…Impaired IFN-g at birth may facilitate skewing of T-cell differentiation toward a Th2 phenotype, thereby predisposing to subsequent development of atopic wheezing and asthma in children (33,34). However, deficient IFN-g may also reflect either decreased maturation of CD8 1 T cells or decreased numbers of NK cells or Th1 cells.…”

Section: Discussionmentioning

confidence: 99%

IFN-γ Production during Initial Infection Determines the Outcome of Reinfection with Respiratory Syncytial Virus

Lee

Miyahara

Takeda

et al. 2008

Am J Respir Crit Care Med

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Rationale: Severe respiratory syncytial virus (RSV) bronchiolitis has been associated with deficient IFN-g production in humans, but the role of this cytokine in determining the outcome of reinfection is unknown. Objectives: To define the role of IFN-g in the development of RSVmediated airway hyperresponsiveness (AHR) and lung histopathology in mice. Methods: Wild-type (WT) and IFN-g knockout mice were infected with RSV in the newborn or weaning stages and reinfected 5 weeks later. Airway responses were assessed on Day 6 after the primary or secondary infection. Measurements and Main Results: Both WT and IFN-g knockout mice developed similar levels of AHR and airway inflammation after primary infection. After reinfection, IFN-g knockout mice, but not WT mice, developed AHR, airway eosinophilia, and mucus hyperproduction. Intranasal administration of IFN-g during primary infection but not during reinfection prevented the development of these altered airway responses on reinfection in IFN-g knockout mice. Adoptive transfer of WT T cells into IFN-g knockout mice before primary infection restored IFN-g production in the lungs and prevented the development of altered airway responses on reinfection. Treatment of mice with IFN-g during primary neonatal infection prevented the enhancement of AHR and the development of airway eosinophilia and mucus hyperproduction on reinfection. Conclusions: IFN-g production during primary RSV infection is critical to the development of protection against AHR and lung histopathology on reinfection. Provision of IFN-g during primary infection in infancy may be a potential therapeutic approach to alter the course of RSV-mediated long-term sequelae.

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Section: Discussionmentioning

confidence: 99%

IFN-γ Production during Initial Infection Determines the Outcome of Reinfection with Respiratory Syncytial Virus

Lee

Miyahara

Takeda

et al. 2008

Am J Respir Crit Care Med

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“…The present authors showed that the capacity of CD4z Th-cells from infants at high risk (HR) of atopy to produce both Th1 and Th2 cytokines was reduced relative to their low risk (LR) counterparts; however, the reduction in IFN-c was greatest, resulting in a relative Th2 "skewing" of responsiveness in the HR children. These findings have since been extended to CBMC in confirmatory studies from a range of independent laboratories [21][22][23][24][25][26].…”

Section: T-cell Immunity To Inhalant Allergens: the Basis Of Variatiomentioning

confidence: 95%

Interactions between respiratory tract infections and atopy in the aetiology of asthma: Fig. 1.—

Holt

Sly²

2002

Eur Respir J

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The prevalence of asthma, in particular atopic asthma, has markedly increased in recent years. Accumulating evidence suggests that environmental factors associated with allergic sensitization and exposure to microbial stimuli during infancy and early childhood, are associated with these changes in prevalence. However, considerable controversy surrounds the role of microbial agents, as evidence has been presented for both positive and negative effects in this context.The review below focuses upon interactions between immune competence during infancy, the development of T-helper (Th)1-polarized versus Th2-polarized memory against inhalant allergens, and susceptibility to virus infection. In particular, recent finding are highlighted which suggest that delayed postnatal maturation of Th1 function is associated with increased risk for early postnatal sensitization to inhalant allergens, and also with risk for viral bronchiolitis during infancy.Variations in the kinetics of postnatal maturation of T-helper 1 function may in part be attributable to polymorphisms in the CD14 gene, which influence host responsiveness both to bacterial as well as viral stimuli. It is evident from a wide range of studies carried out in different geographical areas, that the prevalence of allergic diseases, and in particular atopic asthma, has increased markedly over the last 2-3 decades. Moreover, the increases become evident in successive birth cohorts during early childhood. It is also generally accepted that "diagnostic shift" is not a significant factor in these changes. Accordingly, given the timeframe over which the changes have occurred, the responsible factor(s) must be environmental, presumably interacting with one or more susceptibility genes.The search for the relevant genetic and environmental factors continues, and a variety of potential candidates have been identified. Prominent amongst these are factors related to respiratory infections, particularly those occurring in childhood. Paradoxically, these infections have been invoked both as potential protective factors in relation to asthma/ allergy development, and as triggers of asthma exacerbations in atopic asthmatics. The mechanisms by which these effects may be mediated are incompletely understood; however, recent findings suggest some intriguing new possibilities, which are discussed in this review. T-cell immunity to inhalant allergens: the basis of variations in responder phenotype within the adult populationThe epithelial surface of the upper and lower respiratory tract are continuously exposed to an array of pathogenic and nonpathogenic airborne antigens, and the induction and local expression of local T-cell immunity must accordingly be tightly controlled, in order to avoid the pathological consequences of chronic T-cell-driven inflammation. While it is highly plausible that resistance to airborne pathogens is a direct function of the speed of mobilization and the intensity of expression of local innate and adaptive immune mechanisms in the lung, the conve...

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“…Clinical studies have demonstrated that reduced IFN-␥ secretion in neonates is associated with the subsequent development of atopy (53)(54)(55). Furthermore, a predisposition toward the overproduction of Th1 cytokines may protect against atopy, because patients with multiple sclerosis (56), rheumatoid arthritis (57), or tuberculosis (58), conditions associated with increased production of Th1 cytokines, have a reduced predisposition toward the development of atopy.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of IL-15 In Vivo Enhances Tc1 Response, Which Inhibits Allergic Inflammation in a Murine Model of Asthma

Ishimitsu

Nishimura

Yajima

et al. 2001

The Journal of Immunology

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IL-15, a pleiotropic cytokine, is involved in the inflammatory responses in various infectious and autoimmune diseases. We have recently constructed IL-15-transgenic (Tg) mice, which have an increased number of memory-type CD8+ T cells in the peripheral lymphoid tissues. In the present study, we found that eosinophilia and Th2-type cytokine production in the airway were severely attenuated in OVA-sensitized IL-15-Tg mice following OVA inhalation. IL-15-Tg mice preferentially developed Tc1 responses mediated by CD8+ T cells after OVA sensitization, and in vivo depletion of CD8+ T cells by anti-CD8 mAb aggravated the allergic airway inflammation in IL-15-Tg mice following OVA inhalation. Adoptive transfer of CD8+ T cells from OVA-sensitized IL-15-Tg mice into normal mice before OVA sensitization suppressed Th2 response to OVA in the normal mice. These results suggest that overexpression of IL-15 in vivo suppresses Th2-mediated-allergic airway response via induction of CD8+ T cell-mediated Tc1 response.

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Decreased production of IFN_γ and increased production of IL‐6 by cord blood mononuclear cells of newborns with a high risk of allergy

Abstract: Our data suggested increased production of IL-6 and decreased production of IFN gamma of cord blood mononuclear cells appear to be the hallmark of newborns from the high-risk population.

Cited by 112 publications

References 40 publications

IFN-γ Production during Initial Infection Determines the Outcome of Reinfection with Respiratory Syncytial Virus

IFN-γ Production during Initial Infection Determines the Outcome of Reinfection with Respiratory Syncytial Virus

Interactions between respiratory tract infections and atopy in the aetiology of asthma: Fig. 1.—

Overexpression of IL-15 In Vivo Enhances Tc1 Response, Which Inhibits Allergic Inflammation in a Murine Model of Asthma

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Decreased production of IFNγ and increased production of IL‐6 by cord blood mononuclear cells of newborns with a high risk of allergy

Abstract: Our data suggested increased production of IL-6 and decreased production of IFN gamma of cord blood mononuclear cells appear to be the hallmark of newborns from the high-risk population.

Cited by 112 publications

References 40 publications

IFN-γ Production during Initial Infection Determines the Outcome of Reinfection with Respiratory Syncytial Virus

IFN-γ Production during Initial Infection Determines the Outcome of Reinfection with Respiratory Syncytial Virus

Interactions between respiratory tract infections and atopy in the aetiology of asthma: Fig. 1.—

Overexpression of IL-15 In Vivo Enhances Tc1 Response, Which Inhibits Allergic Inflammation in a Murine Model of Asthma

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Decreased production of IFN_γ and increased production of IL‐6 by cord blood mononuclear cells of newborns with a high risk of allergy