What Cytokines Can Tell Us About the Pathogenesis of Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-ALCL)

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Abstract
Cytokines, their receptors, and downstream signaling partners, especially JAK1/2 and STAT3, are key biomarkers in lymphoproliferative disorders including systemic anaplastic large cell lymphoma (ALCL). Here we review their role in breast implant-associated anaplastic large cell lymphoma (BIA-ALCL). Early results suggest that, in addition to CD30, IL-9, IL-10, and IL-13 can distinguish malignant from benign seromas. IL-6 is increased in both benign and malignant seromas. IFNγ may identify a subset of BIA-ALCL with a different clinical course. Immunohistochemical detection of nuclear transcription factors—which regulate cytokine signaling—and phosphorylated janus kinases/signal transducers and activators of transcription can inform the identification and malignant potential of CD30+ cells. The innate immune response is the first line of defense against microbes suspected to initiate BIA-ALCL. Innate lymphoid cells are grouped according to the cytokines they produce and could potentially be identified as precursors to BIA-ALCL. Cytokines modulate the tumor microenvironment and hence the pathology of BIA-ALCL such as the influx of eosinophils and capsular fibrosis mediated by IL-13. The plasticity of T cells and innate immune cells theoretically can enable therapeutic manipulations toward a less aggressive phenotype. Cytokine receptors targeted in clinical trials of inflammatory and autoimmune disorders could afford opportunities for immunotherapy of BIA-ALCL.

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