2020 年 66 巻 6 号 p. 497-506
Most infants are immunologically active to develop a tolerance to oligoclonal antigens by producing IgA and introducing regulatory T cells in early infancy. Cytokines and their signalling molecules are important mediators in the intestine regulating both oral tolerance and mucosal inflammation. This system works efficiently in most individuals, but for an undefined reason, some people react to food and other proteins as though they were pathogens and induce chronic inflammation as food allergy/intolerance.
The adverse reaction caused by ingested foods is defined as food intolerance. The clinical features of food intolerance include vomiting, diarrhea, bloody stool, eczema, failure to thrive, and a protean range of other symptoms. Intolerance can be divided into two categories depending on whether they are immunologically mediated. The one immunologically mediated is known as “Food allergy”. Food allergy and mucosal inflammation are deeply related since tolerance cannot be introduced when there is an inflammation in the intestinal mucosa. Mast cells, eosinophils, mucosal lymphocytes, and epithelial cells are deeply involved and related each other to cause mucosal inflammation.
Meanwhile, it is known that tolerance can be introduced by keep eating antigenic foods, such as oral desensitization therapy. Feeding lower doses of antigen introduce “active suppression” by inducing TGF-β, IL-4 and IL-10 producing regulatory T (Th3) cells. At higher doses, “clonal anergy” occurs by deleting antigen-specific Th1 and Th2 cells by apoptosis, although TGF-β producing Th3 cells seen spared. These mechanisms are very important for infants to prevent/treat food allergy.
