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Transferrin Disassociates TCR from CD3 Signaling Apparatus to Promote Metastasis.

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Key Laboratory of Genetic Evolution & Animal Models, Key Laboratory of Bioactive Peptides of Yunnan Province, KIZ-CUHK Joint Laboratory of Bioresources and Molecular Research in Common Diseases, National Resource Center for Non-Human Primates, Sino-African Joint Research Center, and New Cornerstone Science Laboratory, Kunming Institute of Zoology, The Chinese Academy of Sciences, Kunming, Yunnan 650201, China.

Immune recognition and activation by the peptide-laden major histocompatibility complex-T cell receptor (TCR)-CD3 complex is essential for anti-tumor immunity. Tumors may escape immune surveillance by dissembling the complex. Here, we report that transferrin, which is overexpressed in patients with liver metastasis, disassociates TCR from the CD3 signaling apparatus by targeting the constant domain (CD) of T cell receptor α (TCRα), consequently suppresses T cell activation, and inhibits anti-metastatic and anti-tumor immunity.

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Monoclonal antibodies (mAbs) improve survival of patients with mature B-cell malignancies. Fcγ-receptor dependent effector mechanisms kill tumor cells but can promote antigen loss through trogocytosis, contributing to treatment failures. Cell-bound mAbs trigger the complement cascade to deposit C3 activation fragments and lyse cells.

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Late-stage eosinophilic myocarditis (or Löffler endocarditis) is known to occur in patients with hypereosinophilic syndrome and can cause restrictive cardiomyopathy. Eosinophilic myocarditis is an acute life-threatening inflammatory disease of the heart that can be associated with cancer. We report a case of a 70-year-old White woman, previously treated for diffuse large B-cell lymphoma in remission, admitted for acute dyspnea with a 1-year history of hypereosinophilia.

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