However, several case reports and small-scale studies have suggested that Bcr-Abl TKIs may be associated with an increased risk of HBV reactivation. Small-molecule inhibitors that target Bcr-Abl tyrosine kinase (Bcr-Abl TKIs, including imatinib, nilotinib, and dasatinib) are standard treatment for chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GISTs). 5, 6, 9 However, there is less information regarding the risks of HBV reactivation associated with targeted therapies, including tyrosine kinase inhibitors (TKIs). 10 Routine HBV screening is recommended before treatment using these medications, and strategies for preventing and treating HBV reactivation are well documented. 7, 8, 9 In this setting, HBV reactivation–related hepatitis or hepatitis B flare is a clinical event that involves an abrupt increase in alanine aminotransferase (ALT) concentrations (to >2-5 times the upper reference limit), and its presentation may vary from asymptomatic to overt acute hepatitis, including hepatic failure. In patients who receive immunosuppressants, HBV reactivation is a well-recognized complication, especially among those who receive high-dose or long-term use of steroids, 4, 5 biologic drugs (eg, rituximab), 6 and chemotherapy. 2 In 1984, Taiwan implemented vaccination programs for infants and high-risk groups, although approximately 15% to 20% of adults still carry HBV. The highest prevalence of HBV infections is in the western Pacific region (6.2% of adults) and Africa (6.1% of adults). Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study collection, management, analysis, and interpretation of the data preparation, review, or approval of the manuscript and decision to submit the manuscript for publication.ĭrug-induced liver injury is an infrequent but challenging complication of drug therapy, 1 and drug-induced hepatitis B virus (HBV) reactivation is particularly important in an HBV endemic area. Arnold Chan at National Taiwan University Hospital. No other disclosures were reported.įunding/Support: Funding was provided by National Taiwan University to the Health Data Research Center and by the research account (MQ3615) of K.
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Arnold Chan, MD, ScD, Health Data Research Center, National Taiwan University, 33 Linsen South Rd, Ste 526, Taipei, Taiwan ( Contributions: Drs Chan and Wang had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.Īcquisition, analysis, or interpretation of data: Wang, Chu, Yang, Chan.Ĭritical revision of the manuscript for important intellectual content: All authors.Īdministrative, technical, or material support: Chu, Lo.Ĭonflict of Interest Disclosures: Dr Chan reported receiving grants from Bayer, Takeda, Amgen, Boehringer Ingelheim, MundiPharma, Merck Sharp and Dohme, and GlaxoSmithKline serving on an advisory committee for Bayer and receiving speaking fees from Amgen outside the submitted work. We also briefly discuss molecular dynamics in this context.Corresponding Author: K. We review downstream analyses, including BCR and TCR epitope prediction, antibody-antigen docking and TCR-peptide-MHC Modeling. After describing the recent sequencing technologies for immune receptor repertoires, we survey structural modeling methods for BCR and TCRs, along with methods for clustering such models. Here, we review recent developments in bioinformatics tools for analysis of BCR and TCR repertoires, with an emphasis on those that incorporate structural features.
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Because the repertoires are highly diverse, specialized software methods are needed to extract meaningful information from BCR and TCR sequence data. The analysis of BCR and TCR repertoires plays an important role in both basic immunology as well as in biotechnology. B cell receptors (BCRs) and T cell receptors (TCRs) make up an essential network of defense molecules that, collectively, can distinguish self from non-self and facilitate destruction of antigen-bearing cells such as pathogens or tumors.
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