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Cow's milk-specific Th2A CD4+ T cells are a specialized subset of pathogenic T helper 2 cells that drive allergic responses to bovine milk proteins. These cells are characterized by a distinct transcriptional profile and the expression of specific surface markers such as CRTH2, CD161, and CD49d, which distinguish them from conventional Th2 cells involved in anti-helminth immunity. In individuals with cow's milk allergy, these cells orchestrate the allergic cascade by producing high levels of pro-inflammatory cytokines like IL-4, IL-5, and IL-13, which promote IgE production and eosinophil activation. They are considered a primary therapeutic target because their frequency and activation state correlate strongly with clinical disease severity and the success of oral immunotherapy (OIT). Successful treatment often results in the deletion or exhaustion of this specific cell population, making them a critical biomarker for monitoring clinical tolerance and the efficacy of emerging allergy biologics.
Therapeutic strategies aim to deplete these cells, induce functional anergy, or promote a phenotypic shift toward a regulatory T cell (Treg) profile through allergen-specific immunotherapy or cytokine signaling blockade.
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