bioRxiv ScienceSearch

Biology subjects

Serrano, M.

Publications and source records attributed to Serrano, M..

3 recordsLinked to original sources

Determining the Quantitative Principles of T Cell Response to Antigenic Disparity: The Case of Stem Cell Transplant Donor-Recipient Exome Wide Mismatching and HLA Bound Alloreactive Peptides

Alloreactivity compromising clinical outcomes in stem cell transplantation is observed despite HLA matching of donors and recipients. This has its origin in the variation between the exomes of the two, which provides the basis for minor histocompatibility antigens (mHA). The mHA presented on the HLA class I and II molecules and the ensuing T cell response to these antigens results in graft versus host disease. In this paper, results of a whole exome sequencing study are presented, with resulting alloreactive polymorphic peptides and their HLA class I and HLA class II (DRB1) binding affinity quantified. Large libraries of potentially alloreactive recipient peptides binding both sets of molecules were identified, with HLA-DRB1 presenting an order of magnitude greater number of peptides. These results are used to develop a quantitative framework to understand the immunobiology of transplantation. A tensor-based approach is used to derive the equations needed to determine the alloreactive donor T cell response from the mHA-HLA binding affinity and protein expression data. This approach may be used in future studies to simulate the magnitude of expected donor T cell response and risk for alloreactive complications in HLA matched or mismatched hematopoietic cell and solid organ transplantation.

immunology

Dynamical System Modeling to Simulate Donor T Cell Response to Whole Exome Sequencing-Derived Recipient Peptides: Understanding Randomness in Clinical Outcomes Following Stem Cell Transplantation

The quantitative relationship between the magnitude of variation in minor histocompatibility antigens (mHA) and graft versus host disease (GVHD) pathophysiology in stem cell transplant (SCT) donor-recipient pairs (DRP) is not established. In order to elucidate this relationship, whole exome sequencing (WES) was performed on 27 HLA matched related (MRD), & 50 unrelated donors (URD), to identify nonsynonymous single nucleotide polymorphisms (SNPs). An average 2,463 SNPs were identified in MRD, and 4,287 in URD DRP (p<0.01); resulting peptide antigens that may be presented on HLA class I molecules in each DRP were derived in silico (NetMHCpan ver2.0) and the tissue expression of proteins these were derived from determined (GTex). MRD DRP had an average 3,670 HLA-binding-alloreactive peptides, putative mHA (pmHA) with an IC50 of <500 nM, and URD, had 5,386 (p<0.01). To simulate an alloreactive donor cytotoxic T cell response, the array of pmHA in each patient was considered as an operator matrix modifying a hypothetical cytotoxic T cell clonal vector matrix; each responding T cell clones proliferation was determined by the logistic equation of growth, accounting for HLA binding affinity and tissue expression of each alloreactive peptide. The resulting simulated organ-specific alloreactive T cell clonal growth revealed marked variability, with the T cell count differences spanning orders of magnitude between different DRP. Despite an estimated, uniform set of constants used in the model for all DRP, and a heterogeneously treated group of patients higher total and organ-specific T cell counts were associated with cumulative incidence of GVHD in recipients in Cox proportional hazard models. In conclusion, exome wide sequence differences and the variable alloreactive peptide binding to HLA in each DRP yields a large range of possible alloreactive donor T cell responses. Our findings also help understand the apparent randomness observed in the development of alloimmune responses.

immunology

Analytical and Clinical Validity Study of FirstStepDx PLUS: A Chromosomal Microarray Optimized for Patients with Neurodevelopmental Conditions

IntroductionChromosomal microarray analysis (CMA) is recognized as the first-tier test in the genetic evaluation of children with developmental delays, intellectual disabilities, congenital anomalies and autism spectrum disorders of unknown etiology.\n\nArray DesignTo optimize detection of clinically relevant copy number variants associated with these conditions, we designed a whole-genome microarray, FirstStepDx PLUS (FSDX). A set of 88,435 custom probes was added to the Affymetrix CytoScanHD platform targeting genomic regions strongly associated with these conditions. This combination of 2,784,985 total probes results in the highest probe coverage and clinical yield for these disorders.\n\nResults and DiscussionClinical testing of this patient population is validated on DNA from either non-invasive buccal swabs or traditional blood samples. In this report we provide data demonstrating the analytic and clinical validity of FSDX and provide an overview of results from the first 7,570 consecutive patients tested clinically. We further demonstrate that buccal sampling is an effective method of obtaining DNA samples, which may provide improved results compared to traditional blood sampling for patients with neurodevelopmental disorders who exhibit somatic mosaicism.\n\nClinical scenarioNeurodevelopmental disabilities, including developmental delays (DD), intellectual disabilities (ID), and autism spectrum disorders (ASD), affect up to 15% of children (1). In the majority of cases, a childs clinical presentation does not allow for a definitive etiological diagnosis. In such cases, CMA is recommended as the first-tier test that should be used to evaluate for a potential genetic etiology (2-7). A definitive genetic diagnosis allows patients to more often receive appropriate medical care tailored to their condition, as reflected by medical management changes and improved access to necessary support and educational services (8-13).\n\nTest descriptionFirstStepDx PLUS (FSDX) is an optimized clinical microarray test provided in the context of a comprehensive clinical service. Testing starts with either a non-invasive buccal swab sample or traditional blood sample from which DNA extraction using a Gentra Puregene(R) kit specific to the sample type (Qiagen, Inc., Valencia, CA) is performed in one of several contracted CLIA/CAP credentialed laboratories according to manufacturers protocols. High quality genomic DNA is fragmented, labeled and hybridized to FSDX arrays using reagents, equipment and methodology as specified by by the manufacturer (Affymetrix, Inc., Santa Clara, CA)(14). Washed arrays are scanned and raw data files are processed to CYCHP files using a reference file comprising at least 100 samples with normal array findings. Data analysis is performed using Chromosome Analysis Suite software version 2.0.1 (Affymetrix). Hybridization of patient DNA to oligonucleotide and SNP probes is independently compared against a previously analyzed cohort of normal samples to call CNVs and allele genotypes. The percentage mosaicism of whole-chromosome aneuploidies is determined using the average log2 ratio of the entire chromosome (14).\n\nMicroarray designFSDX was optimized by the addition of 88,435 custom probes targeting genomic regions strongly associated with ID/DD/ASD (15-24). This was effected, under GMP by Affymetrix, to the CytoScanHD platform using their microarray design process specifications which have been previously described (14). This is consistent with the ACMG recommendation of \"enrichment of probes targeting dosage-sensitive genes known to result in phenotypes consistent with common indications for a genomic screen\" (25). Critical regions that did not meet a desired probe density [&ge;]1 probe/1000 bp on the CytoScanHD were supplemented with additional probe content to allow for improved detection of smaller deletions and duplications in these critical regions. Finally, additional probes were added to improve detection of CNVs encompassing genes involved in other well-characterized neurodevelopmental disorders, for example GAMT (26) and GATM (27). All incremental probes were added in substitution for probes deemed sub-optimal by Affymetrix and previously masked, bringing FSDX to a grand total of 2,784,985 probes. Custom SNP probes (n =416) on FSDX are targeted by 12 oligonucleotides, three for each strand of each allele, which is approximately double the typical probe coverage for SNPs.\n\nTest interpretationCYCHP files are evaluated by ABMG certified cytogeneticists. Determination of CNVs is consistent with established cytogenetic standards. A minimum of 25-consecutive impacted probes is the baseline determinant for deletions and 50 probes for duplications independent of variant size. Rare CNVs are determined to be \"pathogenic\" if there is sufficient evidence published (at least two independent publications) to indicate that haploinsufficiency or triplosensitivity of the region or gene(s) involved is causative of clinical features or of sufficient overall size (28). If however, there is insufficient but at least preliminary evidence for a causative role for the region or gene(s) therein they are classified as variants of unknown significance (VOUS) independent of CNV size. Areas of absence of heterozygosity (AOH) are also classed as VOUS if of sufficient size and location to increase the risk for conditions with autosomal recessive inheritance or conditions with parent-of-origin/imprinting effects. Other CNVs are typically not reported after determination that they most likely represent normal common population variants and are contained in databases documenting presumptively benign CNVs, e.g., the Database of Genomic Variants (DGV) (29). These parameters were standard independent of the microarray used for analysis in comparative studies.\n\nPublic health importanceA definitive genetic diagnosis facilitates patient access to appropriate and necessary medical and support services. Defining the underlying genetic cause of DD/ID/ASD and/or multiple congenital anomalies (MCA) in each unique patient is vital to understanding etiology, prognosis, and course. It informs physicians of potential comorbid conditions for which a patient should be evaluated and treated proactively and optimally. Improved understandings of the appropriate therapeutic and behavioral approaches to that patient are also enabled. Genetic testing is best provided in the context of an integrated service (30), so FSDX provides comprehensive, clear, readable, and personalized reports for the healthcare provider and a family-friendly section to facilitate understanding of the often-complex results. The report is complemented by availability of pre- and post-test genetic counseling and technical support to providers. Moreover, FSDX includes personalized insurance pre-authorization and appeals assistance to overcome barriers encountered by both providers and families that, in many circumstances, prevent access to crucial genetic testing services (10-11).\n\nPublished reviews, recommendations and guidelinesThe American College of Medical Genetics (ACMG) (2,3), the American Academy of Child and Adolescent Psychiatry (4,7), the American Academy of Pediatrics (5), and the American Academy of Neurology/Child Neurology Society (6) recommend CMA as the first-tier test in the genetic evaluation of children with unexplained DD, ID, or ASD. Considerable data supporting these guidelines are documented in numerous reviews and publications (31-36). The ACMG has also published guidelines on both array design (25) and the validation of arrays, including validation of a new version of a platform in use by the laboratory from the same manufacturer, and of additional sample types (28).

genomics