Human subjects without peanut allergy demonstrate T cell–dependent, TH2-biased, peanut-specific cytokine and chemokine responses independent of TH1 expression

Thottingal, Tina B.; Stefura, Bill P.; Simons, F. Estelle R.; Bannon, Gary A.; Burks, Wesley; HayGlass, Kent T.

doi:10.1016/j.jaci.2006.06.016

Cited by 29 publications

(18 citation statements)

References 52 publications

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“…[99][100][101] Allergen-specific cytokine and chemokine production patterns have not yet been used to predict future anaphylactic responses; however, the prevalence and nature of allergen-specific T-cell-dependent cytokine and chemokine responses are being investigated, and useful individual markers or, more likely, a panel of markers may eventually be identified. 150 The development of biomarkers that robustly distinguish between sensitized individuals at risk of foodinduced anaphylaxis and sensitized individuals who can tolerate the food remains a major unmet need.…”

Section: Risk Assessment In Individuals Sensitized To Foodsmentioning

confidence: 99%

Risk assessment in anaphylaxis: Current and future approaches

Simons

Frew

Ansotegui

et al. 2007

Journal of Allergy and Clinical Immunology

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262

300

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Section: Risk Assessment In Individuals Sensitized To Foodsmentioning

confidence: 99%

Risk assessment in anaphylaxis: Current and future approaches

Simons

Frew

Ansotegui

et al. 2007

Journal of Allergy and Clinical Immunology

Self Cite

262

300

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“…All subjects were Th1-biased in response to nonallergic foods, suggesting an association between Th1 response and allergy resolution. In a subsequent study, Thottingal et al argued against the idea of a protective Th1 bias in healthy individuals after finding insignificant differences in Th1 response between healthy and allergic subjects [54]. Taken together, these studies suggest allergen sensitivity does not innately alter the immune system, but instead determines immune response.…”

Section: Diagnostic Tools For Famentioning

confidence: 99%

Food Allergy Diagnosis and Therapy: Where are we Now?

2013

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Food allergy is a growing worldwide epidemic that adversely effects up to 10% of the population. Causes and risk factors remain unclear and diagnostic methods are imprecise. There is currently no accepted treatment for food allergy. Therefore, there is an imminent need for greater understanding of food allergies, revised diagnostics and development of safe, effective therapies. Oral immunotherapy provides a particularly promising avenue, but is still highly experimental and not ready for clinical use.

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“…Levels of IgE, originally a defense mechanism against worms, are increased in the blood of allergic patients during the so-called IgE-mediated hypersensitivity, where the IgE response is attributed to the generation of TH2 cells that produce IL-4, IL-5 and IL-13 [11]. …”

Section: Pathophysiologymentioning

confidence: 99%

Food Allergy: Recent Advances in Pathophysiology and Diagnosis

Dupont

2011

Ann Nutr Metab

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Approximately 5% of young children and 3–4% of adults exhibit adverse immune responses to foods in westernized countries, with a tendency to increase. The pathophysiology of food allergy (FA) relies on immune reactions triggered by epitopes, i.e. small amino-acid sequences able to bind to antibodies or cells. Some food allergens share specific physicochemical characteristics that allow them to resist digestion, thus enhancing allergenicity. These allergens encounter specialized dendritic cell populations in the gut, which leads to T-cell priming. In case of IgE-mediated allergy, this process triggers the production of allergen-specific IgE by B cells. Tissue-resident reactive cells, including mast cells, then bind IgE, and allergic reactions are elicited when these cells, with adjacent IgE molecules bound to their surface, are re-exposed to allergen. Allergic reactions occurring in the absence of detectable IgE are labeled non-IgE mediated. The abrogation of oral tolerance which leads to FA is likely favored by genetic disposition and environmental factors (e.g. increased hygiene or enhanced allergenicity of some foods). For an accurate diagnosis, complete medical history, laboratory tests and, in most cases, an oral food challenge are needed. Noticeably, the detection of food-specific IgE (sensitization) does not necessarily indicate clinical allergy. Novel diagnostic methods currently under study focus on the immune responses to specific food proteins or epitopes of specific proteins. Food-induced allergic reactions represent a large array of symptoms involving the skin and gastrointestinal and respiratory systems. They can be attributed to IgE-mediated and non-IgE-mediated (cellular) mechanisms and thus differ in their nature, severity and outcome. Outcome also differs according to allergens.

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Human subjects without peanut allergy demonstrate T cell–dependent, TH2-biased, peanut-specific cytokine and chemokine responses independent of TH1 expression

Cited by 29 publications

References 52 publications

Risk assessment in anaphylaxis: Current and future approaches

Risk assessment in anaphylaxis: Current and future approaches

Food Allergy Diagnosis and Therapy: Where are we Now?

Food Allergy: Recent Advances in Pathophysiology and Diagnosis

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