Los Angeles | Consumption of a normal diet stimulates cells in the gut that suppress rejection of food by the immune system, scientists have found, explaining why some children are more susceptible to food allergies. Food allergy or intolerance can cause symptoms ranging from a harmless skin rash to a potentially lethal anaphylactic shock.
Researchers from La Jolla Institute for Allergy and Immunology (LJI) in US have explained how food tolerance emerges over time in normal individuals. Coupling molecular approaches with a long-forgotten model of ‘antigen-free’ mice, the study is the first to demonstrate that consumption of a normal diet stimulates cells in the gut that suppress rejection of food by the immune system. Knowing this could explain why children, who have more limited exposure to novel foods than adults, are more susceptible to food allergies.
Like pathogens, food displays macromolecular markers known as antigens that announce to the immune system that food is ‘foreign’. Previous analysis of how the body distinguishes antigenic friend from foe revealed that feeding lab mice a novel test protein – for example, the egg protein ovalbumin – induced development of immunosuppressive T-regulatory, or ‘Treg’ cells, in the gut, which then acted to block the immune response to that particular protein.
Researchers re-established ‘antigen-free’ mouse models designed to represent an immunological blank slate. These animals were not only raised in a germ-free environment but were also fed an ‘elemental’ diet of amino acids, the building blocks of proteins, rather than foods that contain intact proteins themselves.
The mice were, in essence, immunologically naive, because the amino acid building blocks are too small to be recognised by the immune system.
These mice therefore have little or no prior contact with antigenic proteins and other macromolecules. Using molecular marker analysis, researchers found that antigen-free mice were depleted of Tregs in the small intestine whereas a large number of these Tregs were present in germ-free counterparts fed a ‘normal’ protein diet.
That difference alone suggested that proteins contained in food stimulate Treg development. It also hinted that Tregs present in the gut of normal mice might suppress a potentially disastrous immune response to those proteins. Our work shows food tolerance is acquired and involves specific populations of T cells that develop following its consumption.
Without them, we would mount a strong immune response to macromolecules contained in food, said Charles Surh from LJI.
The study suggests what happens on a cellular basis as some children outgrow it – they may be expanding their repertoire of Tregs that recognise new foods as ‘safe’.
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