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Peanut-responsive CD4+ T cells are a specialized subset of helper T lymphocytes that recognize peanut-derived allergens, such as Ara h 1, 2, and 3, via their T-cell receptors (Wambre et al., 2017, Science Translational Medicine). In individuals with peanut allergy, these cells predominantly exhibit a pathogenic Th2 phenotype, often referred to as Th2A cells, which are characterized by the expression of markers like CRTH2 and CD161 (Ryan et al., 2020, Journal of Allergy and Clinical Immunology). These cells drive the allergic cascade by secreting pro-inflammatory cytokines, including IL-4, IL-5, and IL-13, which promote IgE class switching in B cells and recruit effector cells like eosinophils. The activation of these T cells upon peanut exposure is the primary driver of clinical symptoms ranging from urticaria to systemic anaphylaxis. Therapeutic strategies, such as oral immunotherapy (OIT), aim to modulate these cells by inducing a state of desensitization or long-term tolerance (Vickery et al., 2013, Journal of Allergy and Clinical Immunology). This modulation often involves the induction of regulatory T cells (Tregs) or the functional exhaustion and deletion of the pathogenic Th2 subset. Monitoring the frequency and cytokine profile of these cells serves as a vital biomarker for assessing the efficacy of emerging allergy treatments (FDA, 2020, Palforzia Prescribing Information).
Induction of immune tolerance, Th2 to Th1/Treg immune deviation, T-cell anergy, and inhibition of Th2 cytokine signaling.
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