{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTNFRSF8 (CD30) is a transmembrane receptor of the tumor necrosis factor receptor superfamily that was originally identified on malignant cells in Hodgkin lymphoma and is now recognized as being expressed on a variety of hematologic malignancies and activated lymphocytes. In diffuse large B‐cell lymphoma, for example, its expression has been linked to a favorable prognosis and a distinct gene expression signature, while in Hodgkin’s disease, ligand‐independent self‐aggregation of CD30 triggers the recruitment of adaptor molecules to activate NF‐κB and drive cytokine production. CD30 is also a diagnostic marker in conditions such as systemic mastocytosis and cutaneous lymphoproliferative disorders, and its aberrant expression and clonality have provided insight into the cellular origins and potential progression of diseases such as mycosis fungoides and lymphomatoid papulosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, CD30 signaling is complex and context dependent. In Hodgkin’s cells, ligand‐independent CD30 stimulation mediates the activation of NF‐κB through the recruitment of TRAF proteins and other adaptors, forming a survival circuitry that may also involve a regulatory interplay with redox catalysts such as thioredoxin-1. Promoter studies have identified that factors such as JunB can relieve transcriptional repression of the CD30 gene, leading to its overexpression, while proteolytic shedding of its ectodomain by metalloproteases (for example, ADAM10) and incorporation into extracellular vesicles help modulate its availability and intercellular signaling. Such molecular mechanisms underpin both the ability of CD30 to regulate downstream gene expression (which balances cell survival and apoptosis) and its role as a target for antibody–drug conjugates in diseases like anaplastic large cell lymphoma."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}, {"type": "fg_f", "ref": "19"}, {"type": "fg_f", "ref": "13"}, {"type": "fg_f", "ref": "20"}, {"type": "fg_f", "ref": "18"}, {"type": "fg_f", "ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in neoplasia, CD30 functions in normal immune regulation and in pathologic immune responses. Soluble CD30 levels in serum have been employed as an indicator of T‐cell activation in conditions ranging from transplant rejection and HIV persistence to autoimmune diseases such as systemic lupus erythematosus and even in pregnancy complications. In addition, studies in eosinophils have demonstrated that CD30 engagement can induce apoptosis, suggesting a role in modulating inflammatory cell survival in allergic diseases. Together, these diverse findings underscore CD30’s significance as both a biomarker and a therapeutic target in multiple clinical settings where immune activation and regulation are perturbed."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Shimin Hu, Zijun Y Xu-Monette, Aarthi Balasubramanyam, et al. 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