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Cow’s Milk Allergy: A Complex Disorder

Ross G. Crittenden, PhD and Louise E. Bennett, PhD

Food Science Australia, Werribee, Victoria, AUSTRALIA



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Fig. 1. Cow’s milk allergy is distinct from cow’s milk intolerances such as lactose intolerance and is caused by an aberrant inflammatory immune response to milk proteins. CMA is also not a single disease, but possibly involves a spectrum of immunological mechanisms. It is generally classified into IgE-mediated allergy and non-IgE-mediated allergy.

 


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Fig. 2. Mechanisms of allergic reactions to milk proteins. Milk proteins are pinocytosed by antigen presenting cells (APC) and peptide epitopes are presented to T cells. Dendritic cells are an important class of APCs with a strong ability to program naive T cells. In IgE-mediated allergy, Th2 effector T cells signal B cells via interleukin-4 (IL-4) to class switch antibody production to allergenic milk protein-specific IgE, which then binds to, and arms, mast cells (sensitization). Milk proteins cross-linking the IgE on armed mast cells cause cell degranulation and rapid release of powerful inflammatory mediators (activation). Non-IgE-mediated mechanisms are poorly understood, but may involve activation of inflammatory cells via interferon-gamma (IFN-{gamma}). Oral tolerance is achieved by T cell anergy, or by the action of regulatory T cells (T reg) that suppress the action of effector T cells (Th1 and Th2) via interleukin-10 (IL-10), transforming growth factor-beta (TGF-ß), or cell-to-cell contact.

 





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