HLA-A*01:354 differs from HLA-A*01:01:01:01 by a single nonsynonymous change (124G->A, glycine 18 to arginine).
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Dynamic allostery in the peptide/MHC complex enables TCR neoantigen selectivity.
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January 2025
Department of Chemistry and Biochemistry, University of Notre Dame, Notre Dame, IN, USA.
The inherent antigen cross-reactivity of the T cell receptor (TCR) is balanced by high specificity. Surprisingly, TCR specificity often manifests in ways not easily interpreted from static structures. Here we show that TCR discrimination between an HLA-A*03:01 (HLA-A3)-restricted public neoantigen and its wild-type (WT) counterpart emerges from distinct motions within the HLA-A3 peptide binding groove that vary with the identity of the peptide's first primary anchor.
View Article and Find Full Text PDFIdentification of the Novel HLA-A*02:1098 Allele by Sanger Dideoxy Nucleotide Sequencing in a Chinese Individual.
HLA
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Department of Laboratory Medicine, College of Health Science and Technology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
The HLA-A*02:1098 allele differs from HLA-A*02:07:01:01 by a single non-synonymous nucleotide change in exon 3.
View Article and Find Full Text PDFIdentification of novel KRAS neoantigen specific TCRs and a strategy to eliminate off-target recognition.
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January 2025
Department of Breast and Thyroid Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Background: T cell receptor (TCR)-engineered T cells targeting neoantigens originated from mutations in KRAS gene have demonstrated promising outcomes in clinical trials against solid tumors. However, the challenge lies in developing tumor-specific TCRs that avoid cross-reactivity with self-antigens to minimize the possibility of severe clinical toxicities. Current research efforts have been put towards strategies to eliminate TCR off-target recognition.
View Article and Find Full Text PDFDepletion of alloreactive B cells by drug- resistant chimeric alloantigen receptor T cells to prevent transplant rejection.
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Institute of Transfusion Medicine and Transplant Engineering, Hannover Medical School; 30625 Hannover, NI, Germany. Electronic address:
Antibody-mediated rejection (AMR) remains a major complication after solid organ transplantation (SOT). Current treatment options are inefficient and result in drastic impairment of the general immunity. To selectively eliminate responsible alloreactive B cells characterized by anti-donor-HLA B-cell receptors (BCRs), we generated T cells overcoming rejection by antibodies (CORA-Ts) engineered with a novel chimeric receptor comprising a truncated donor-HLA molecule as antigen recognition domain.
View Article and Find Full Text PDFNovel Therapeutics in Soft Tissue Sarcoma.
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Sarcoma Unit, The Royal Marsden Hospital and Institute of Cancer Research, London SW3 6JZ, UK.
There has been noteworthy progress in molecular characterisation and therapeutics in soft tissue sarcomas. Novel agents have gained regulatory approval by the FDA. Examples are the tyrosine kinase inhibitors avapritinib and ripretinib in gastrointestinal stromal tumours (GIST), the immune check point inhibitor atezolizumab in alveolar soft part tissue sarcoma, the γ-secretase inhibitor nirogacestat in desmoid tumours, the NTRK inhibitors larotrectinib and entrectinib in tumours with fusions, the mTOR inhibitor nab-sirolimus in PEComa, and the EZH-2 inhibitor tazemetostat in epithelioid sarcoma.
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