Figure 4.

Proposed hypothesis for progression of immune T-cell infiltrates to breast implant–associated anaplastic large-cell lymphoma (BIA-ALCL). In this proposed model, a triggering event elicits both innate and adaptive [type 17 helper T-cell (Th17)/Th1/Th2] immune responses. Oncogenic events, including critical mutations leading to constitutive Janus kinase (JAK)–STAT activation and/or other oncogenic drivers, result in the emergence of monoclonal, CD30-positive BIA-ALCL cells capable of amplifying the inflammatory environment through plasticity and secretion of cytokines, leading to infiltration of eosinophils (Eos) and IgE-coated mast cells (MC). *Variable reports of IL-17 expression in the literature. IFN-γ, interferon-γ; pSTAT3, phospho-STAT3.