TH2-polarized immunological memory to inhalant allergens in atopics is established during infancy and early childhood

YABUHARA, A.; Macaubas, Claudia; Prescott, Susan L.; VENAILLE, T. J.; Holt, B.J.; HABRE, W.; Sly, Peter D.; Holt, Patrick G.

doi:10.1046/j.1365-2222.1997.990906.x

Cited by 105 publications

(155 citation statements)

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“…Firstly, these show that initial low-level responses in CBMC are dominated by Th2 cytokines [13], but are subsequently modified during infancy and early childhood. Thus, Th2 reactivity is steadily boosted in children who progress to early expression of atopy symptoms [14] and/or skin-prick test positivity to inhalants [17,18]; whereas, these responses are diverted ("immune deviated") towards a Th1-like pattern in the nonatopics. This Th memory generation process in many individuals appears to be complete by the end of the preschool or early school years, potentially locking individuals into lifelong patterns of allergen responsiveness.…”

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

confidence: 99%

“…The following principal observations underpin the atopy component of this scheme. 1) Allergen-specific Th-cell priming occurs in the perinatal period [8][9][10][11][12][13], and these early immune responses become compartmentalized into Th1-or Th2-polarized memory during the preschool years [14][15][16][17][18].…”

Section: The Apparent Dualistic Effects Of Respiratory Tract Infectiomentioning

confidence: 99%

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

confidence: 99%

Section: The Apparent Dualistic Effects Of Respiratory Tract Infectiomentioning

confidence: 99%

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

Holt

Sly²

2002

Eur Respir J

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“…Short fetal CDR3 regions may result in flat Agbinding sites (13). This may explain the frequent presence of lowaffinity polyreactive specificities in naive frequent thymic emigrants in the fetal immune system (14,15). This low-affinity response is illustrated in T cell epitope mapping of OVA, a common food allergen, in cord compared with adult blood.…”

mentioning

confidence: 99%

“…This low-affinity response is illustrated in T cell epitope mapping of OVA, a common food allergen, in cord compared with adult blood. CBMC demonstrate broadly reactive responses to multiple OVA peptides that are absent in adults (15), suggesting fetal lymphocytes' lack of fine antigenic specificity to certain Ags.…”

mentioning

confidence: 99%

Fine Specificity of Neonatal Lymphocytes to an Abundant Malaria Blood-Stage Antigen: Epitope Mapping ofPlasmodium falciparumMSP133

Malhotra

Wamachi

Mungai

et al. 2008

The Journal of Immunology

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Cord blood T cells have been reported to respond to a variety of exogenous Ags, including environmental allergens and various viruses and parasites, as demonstrated by enhanced proliferation and cytokine secretion. This finding is evidence that Ags in the maternal environment transplacentally prime and result in fetal development of memory T cells. Some studies suggest these neonatal T cell responses may arise by nonspecific activation of T cells that express TCRs with low binding affinity, thus lacking fine lymphocyte specificity. To address this question, we examined malaria Ag stimulation of human cord and adult blood mononuclear cells in samples from residents of a malaria endemic area in Kenya. We constructed overlapping 18-mer peptides derived from sequences contained in dimorphic alleles of the C-terminal 33-kDa fragment of Plasmodium falciparum merozoite protein 1. This study identified a dominant T cell epitope for one MSP133 allele (MAD20) and two T cell epitopes for the second allele (K1); these epitopes were nonoverlapping and allele specific. In a given donor, peptide-specific proliferation and IFN-γ secretion were highly concordant. However, IL-10 and IL-13 secretion were not correlated. Importantly, the fine specificity of lymphocyte proliferation and cytokine secretion in cord and adult blood mononuclear cells was similar. Cord blood cells obtained from malaria-infected pregnant women were 4-fold more likely to acquire a peptide-specific immune response. We conclude that the fetal malaria response functions in a fully adaptive manner and that this response may serve to help protect the infant from severe malaria during infancy.

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“…Another study revealed a predominant CD4+ positive T cells, eosinophil rich infiltrate and increased IgE response which suggests a Thelper 2 (T-h2) mediated response to the salivary protein 5 . Moreover atopic individuals have a high IgE production and a persistent Th2 response (6)(7).…”

Section: Mechanism Of Papular Urticariamentioning

confidence: 99%

Papular Urticaria: A Known Early Indicator of Atopic Dermatitis

Thomas¹,

Ravi²

2017

ARC Journal of Dermatology

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TH2-polarized immunological memory to inhalant allergens in atopics is established during infancy and early childhood

Cited by 105 publications

References 0 publications

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

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

Fine Specificity of Neonatal Lymphocytes to an Abundant Malaria Blood-Stage Antigen: Epitope Mapping ofPlasmodium falciparumMSP133

Papular Urticaria: A Known Early Indicator of Atopic Dermatitis

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