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10.1038/s41598-017-10265-6

http://scihub22266oqcxt.onion/10.1038/s41598-017-10265-6
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suck abstract from ncbi


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pmid28855662
      Sci+Rep 2017 ; 7 (1 ): 9923
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  • TCR-like antibodies mediate complement and antibody-dependent cellular cytotoxicity against Epstein-Barr virus-transformed B lymphoblastoid cells expressing different HLA-A*02 microvariants #MMPMID28855662
  • Lai J ; Choo JAL ; Tan WJ ; Too CT ; Oo MZ ; Suter MA ; Mustafa FB ; Srinivasan N ; Chan CEZ ; Lim AGX ; Zhong Y ; Chan SH ; Hanson BJ ; Gascoigne NRJ ; MacAry PA
  • Sci Rep 2017[Aug]; 7 (1 ): 9923 PMID28855662 show ga
  • Epstein-Barr virus (EBV) is a common gammaherpesvirus associated with various human malignancies. Antibodies with T cell receptor-like specificities (TCR-like mAbs) provide a means to target intracellular tumor- or virus-associated antigens by recognising their processed peptides presented on major histocompatibility complex (MHC) class I (pMHC) complexes. These antibodies are however thought to be relevant only for a single HLA allele. Here, we show that HLA-A*02:01-restricted EBV antigenic peptides EBNA1(562-570), LMP1(125-133) and LMP2A(426-434) display binding degeneracy towards HLA-A*02 allelic microvariants, and that these pMHC complexes are recognised by anti-EBV TCR-like mAbs E1, L1 and L2 raised in the context of HLA-A*02:01. These antibodies bound endogenously derived pMHC targets on EBV-transformed human B lymphoblastoid cell lines expressing A*02:01, A*02:03, A*02:06 and A*02:07 alleles. More importantly, these TCR-like mAbs mediated both complement-dependent and antibody-dependent cellular cytotoxicity of these cell lines in vitro. This finding suggests the utility of TCR-like mAbs against target cells of closely related HLA subtypes, and the potential applicability of similar reagents within populations of diverse HLA-A*02 alleles.
  • |Antibodies, Monoclonal/*metabolism [MESH]
  • |Antibody-Dependent Cell Cytotoxicity [MESH]
  • |Cell Line, Tumor [MESH]
  • |Genetic Variation [MESH]
  • |HLA-A2 Antigen/chemistry/*genetics/immunology [MESH]
  • |Herpesviridae Infections/immunology [MESH]
  • |Herpesvirus 4, Human/*immunology [MESH]
  • |Humans [MESH]
  • |Models, Molecular [MESH]
  • |Peptide Fragments/metabolism [MESH]


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