Reduced interferon-γ but normal IL-4 and IL-5 release by peripheral blood mononuclear cells from Xhosa children with atopic asthma

Nurse, Barbara; Haus, Matt; Puterman, A.; Weinberg, Eugene; Potter, Paul

doi:10.1016/s0091-6749(97)70171-4

Cited by 42 publications

(47 citation statements)

References 46 publications

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“…Consistently, T-bet-deficient mice have impaired IFN-γ production and also develop spontaneous AHR similar to allergic patients (Finotto et al 2002). Also, T-bet expression in CD4 + T cells is diminished in the lungs of asthmatic patients, who present sig- nificantly lower IFN-γ secretion by peripheral blood mononuclear cells when compared with healthy individuals (Nurse et al 1997, Finotto et al 2002. On the other hand, the Th2-induced transcription factor GATA-3 specifically controls the expression of Th2 cytokines, which are essential to induce allergic inflammation in vivo (Zheng & Flavell 1997).…”

Section: Ifn-γ γ γ γ γ and Th Immune Responsementioning

confidence: 68%

The role of interferon-gamma on immune and allergic responses

Teixeira

Fonseca

Barboza

et al. 2005

Mem. Inst. Oswaldo Cruz

114

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Section: Ifn-γ γ γ γ γ and Th Immune Responsementioning

confidence: 68%

The role of interferon-gamma on immune and allergic responses

Teixeira

Fonseca

Barboza

et al. 2005

Mem. Inst. Oswaldo Cruz

114

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“…However, insufficient localization of Th1 cells is a plausible explanation for enhanced reactivity in the CCR2 Ϫ/Ϫ mutants, in view of the above-mentioned IFN-␥ suppression of Th2 responses (40,41). In support of the notion that IFN-␥ activity may influence Th2 activity, chemokine profiles of children with atopic asthma reveal correlation of disease with low IFN-␥ activity (43). These observations raise the question of whether enhanced airway responses and inflammation in the CCR2 mutants is directly related to factors that induce Th2 polarization or indirectly related to diminished Th1 activity with reduced levels of IFN-␥.…”

Section: Figure 12mentioning

confidence: 75%

Enhanced Airway Th2 Response After Allergen Challenge in Mice Deficient in CC Chemokine Receptor-2 (CCR2)

Kim

Sung

Kuziel

et al. 2001

The Journal of Immunology

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To evaluate the role of CCR2 in allergic asthma, mutant mice deficient in CCR2 (CCR2−/−) and intact mice were sensitized with i.p. OVA with alum on days 0 and 7, and challenged by inhalation with nebulization of either OVA or saline. Airway hyperreactivity, measured by the methacholine-provoked increase in enhanced pause, was significantly increased (p < 0.05) in OVA-challenged CCR2−/− mutant mice, compared with comparably challenged CCR2+/+ mice. OVA-challenged CCR2−/− mutants also were also found to have enhanced bronchoalveolar lavage fluid eosinophilia, peribronchiolar cellular cuffing, and Ig subclass switching, with increase in OVA-specific IgG1 and IgE. In addition, RNase protection assay revealed increased whole lung expression of IL-13 in OVA-challenged CCR2−/− mutants. Unexpectedly, serum monocyte chemotactic protein-1 levels were 8-fold higher in CCR2−/− mutants than in CCR2+/+ mice sensitized to OVA, but OVA challenge had no additional effect on circulating monocyte chemotactic protein-1 in either genotype. Ag stimulation of lymphocytes isolated from OVA-sensitized CCR2 mutants revealed a significant increase (p < 0.05) in IL-5 production, which differed from OVA-stimulated lymphocytes from sensitized CCR2+/+ mice. These experiments demonstrate an enhanced response in airway reactivity and in lung inflammation in CCR2−/− mutant mice compared with comparably sensitized and challenged CCR2+/+ mice. These observations suggest that CC chemokines and their receptors are involved in immunomodulation of atopic asthma.

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“…The involvement of a common part of the immune system for each of these processes is emphasised by a number of studies showing that immunological factors associated with increased host protection from parasite disease are also associated with increased asthma. For example, reduced IFN-c secretion from PBMC has not only been associated with more severe helminthic infection, as mentioned above, but it has also been reported to be associated with asthma in a study of Xhosa children from South Africa [16]. The same variant of STAT6 that has been associated with a reduced burden of ascaris infection has been associated with asthma [17].…”

Section: Comparison Between Mechanisms Of Immune Function For Host Prmentioning

confidence: 86%

Evolution and respiratory genetics

Souëf¹,

Candelaria²,

Goldblatt³

2006

European Respiratory Journal

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Evolution is a plausible explanation for between-population differences in particular allele frequencies if: the genes involved have related functions; the heterogeneous alleles involved have similar functional consequences; the involved genes are not linked chromosomally; and the patterns observed would result in a biologically plausible, survival-enhancing geneenvironment interaction. However, possible evolutionary effects have to be differentiated from founder effects and random genetic drift.The current authors have noted the existence of a consistent pattern of allelic frequencies in genes related to T-helper 2 (Th2) immune responses in humans of different ancestral backgrounds, residing in climatically similar regions. Th2 responses are thought to have evolved in mammals to resist infection by parasites, particularly helminths. Modern man arose in tropical Africa where helminths thrived. Relatively recently, humans migrated to cooler or drier climates where most helminths struggled to reproduce. The genetic tendency to strong Th2 responses may have become a health liability, the reduction in risk from parasites being counterbalanced by an increased inherited propensity to atopic or allergic diseases.The pattern noted by the present authors includes specific alleles of interleukin-4 and its receptor, interleukin-13, interleukin-10, the b chain of the high-affinity receptor for immunoglobulin E, the b 1 -adrenergic receptor, and the alpha chain of tumour necrosis factor. These population-specific polymorphism profiles are likely to be relevant in current disease patterns. The high incidence of asthma in migrants from tropical locations to affluent temperate countries is likely to be related to these patterns. Of even more concern is the possibility that increasing westernisation among the ,2 billion people living in the tropics will produce rapidly increasing levels of asthma, as these populations have a high genetic predisposition to allergic disease.

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Reduced interferon-γ but normal IL-4 and IL-5 release by peripheral blood mononuclear cells from Xhosa children with atopic asthma

Cited by 42 publications

References 46 publications

The role of interferon-gamma on immune and allergic responses

The role of interferon-gamma on immune and allergic responses

Enhanced Airway Th2 Response After Allergen Challenge in Mice Deficient in CC Chemokine Receptor-2 (CCR2)

Evolution and respiratory genetics

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