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Cow's milk-specific FOXP3+ regulatory CD4+ T cells are a specialized subset of immune cells essential for maintaining oral tolerance to bovine milk proteins such as casein and beta-lactoglobulin (Ruiter et al., 2007, PubMed). These cells are defined by the expression of the transcription factor FOXP3, which acts as a master regulator for their suppressive phenotype and function (Fontenot et al., 2003, Nature Immunology). In patients with cow's milk allergy (CMA), there is a functional deficiency or reduced frequency of these specific Tregs, allowing for an exaggerated Th2-mediated allergic response characterized by high IgE production (Tordesillas et al., 2017, Lancet). Therapeutic strategies, most notably oral immunotherapy (OIT), target these cells by providing controlled allergen exposure to induce their expansion and activation (Shreffler et al., 2009, JACI). Once activated, these Tregs secrete inhibitory cytokines like IL-10 and TGF-beta, which suppress effector T cells and promote the production of protective IgG4 antibodies by B cells (Ndhlovu et al., 2015, Scientific Reports). Monitoring the levels and activity of these cells is critical for assessing the efficacy of immunotherapy and the achievement of sustained unresponsiveness in allergic individuals (Varshney et al., 2011, JACI).
Induction of allergen-specific immune tolerance by expanding and activating FOXP3+ regulatory T cells that suppress Th2-mediated allergic inflammation and promote the production of protective IgG4 antibodies.
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