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Robins, H.

Publications and source records attributed to Robins, H..

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TACO: An open, interpretable model for microsecond-scale TCR specificity prediction

Predicting antigen-induced T-cell activation from T-cell receptor (TCR) and peptide sequence remains difficult for TCRs and peptides not represented in training data. We present TACO (T-Cell Activation from Chemistry and Orientation), an open statistical model for predicting TCR specificity against HLA-A*02:01-presented peptides. TACO takes as input the peptide sequence and six TCR CDR loop sequences. Learning from binary activation labels, TACO selects a single canonical orientation of the CDR loops over the peptide and learns five amino-acid contact-potential matrices as well as two peptide-exposure profiles.The orientation is fixed and does not require experimentally determined or predicted structures. We evaluate TACO on held-out peptides separated by Levenshtein distance at least four from all training and validation peptides, limiting near-neighbor shortcut learning. TACO achieves AUROC 0.67 on a large held-out activation dataset and 0.68 on IMMREP25 HLA-A*02:01, exceeding the open structure-based models evaluated here and matching the reported AlphaFold3-TCRdock result. The model has 2,019 fitted parameters, retains most within-peptide ranking signal with TCR$\beta$ sequence alone, and reaches 406,000 TCR--peptide predictions per second on CPU. This throughput enables computational evaluation of large TCR-peptide search spaces. We show its potential use for prioritizing candidate target peptides from large peptide libraries, reducing the search space for downstream experimental investigation. TACO fitted parameters also expose candidate physicochemical patterns that can be inspected directly. We release TACO's parameters and complete training, evaluation, and inference code.

immunology↗

HLAResolver: A statistical framework for resolving HLA ambiguity in T-cell response data

Large-scale models of T-cell recognition require training examples that specify the complete T-cell receptor (TCR)-peptide-human leukocyte antigen (HLA) complex. Multiplexed Identification of T-cell Receptor Antigen Specificity (MIRA) is a high-throughput assay that identifies TCRs associated with responses to specific peptides, but does not determine which HLA presents each peptide. Because a donor can carry up to six distinct class I HLA-A, HLA-B, and HLA-C alleles, each response may have several candidate presenting HLAs. To narrow this set of candidate presenting HLAs, we developed HLAResolver, a statistical framework that combines MIRA response patterns across HLA-typed donors with NetMHCpan predictions of peptide presentation. For each peptide, HLAResolver uses negative-binomial regression to jointly estimate associations between HLA alleles and TCR response counts, accounting for differences in assay yield. NetMHCpan eluted-ligand predictions guide sparse regularization, favoring alleles with stronger predicted presentation while allowing strong MIRA response evidence to support alternatives. To assess whether this integration provides an advantage over either approach alone, we compared HLAResolver with NetMHCpan, which predicts peptide-HLA presentation, and the Restrictor Analysis Tool for Epitopes (RATE), which infers HLA associations from T-cell response patterns. Using held-out MIRA experiments, we assessed each method's ability to predict observed responses and the number of candidate HLAs it assigned. At matched specificity for predicting MIRA responses, HLAResolver achieved higher sensitivity while selecting fewer candidate HLAs per peptide than either comparator.

immunology↗

HLA Alleles Imprint Distinct Biases in the Usage Preferences of TCR Vβ segments

T cells must co-recognize peptide and HLA, yet the extent to which this specificity is shaped by germline-encoded TCR-HLA contacts versus selection during thymic development has remained difficult to quantify. Leveraging population-scale TCR{beta} repertoires linked to donor HLA genotypes, we construct allele-specific V{beta} usage profiles and normalize them to repertoire-wide baselines to derive interpretable HLA-TCR V{beta} preference vectors. We demonstrate that different HLA alleles imprint distinct biases in the usage frequency of TCR V{beta} gene segments among the public TCRs that engage those alleles; consistent with germline-encoded TCR-HLA contact preferences, certain V{beta} genes are over-represented for particular HLA alleles. Similarities in HLA amino-acid sequence predict similarities in both their V{beta} preferences and peptide-binding motifs; a residue-level analysis disentangles HLA positions primarily associated with TCR engagement from those associated with peptide motifs. The TCR-associated HLA positions localize to canonical TCR-facing helices, whereas peptide-associated HLA positions track binding pockets, revealing distinct molecular routes by which HLA polymorphism shapes the TCR and peptide sides of recognition. CMV exposure stratifications confirmed these patterns are not explained by a few dominant infections. Together, these data support that germline-encoded constraints set the landscape of TCR-HLA compatibility, while thymic and peptide-driven forces tune the realized repertoire. These HLA-specific V{beta} biases are a biological prior that should provide a baseline for better understanding of TCR-pHLA specificity as a whole and should be accounted for in future evaluation of any TCR-pHLA specificity prediction methods.

immunology↗

A Fundamental Relationship between TCR Diversity, Repertoire Size and Systemic Clonal Expansion: Insights from 30,000 TCRβ Repertoires

TCR diversity is essential for immune defense, yet the mechanisms underlying its decline with age, its dependence on sex and its variation among individuals remain poorly understood. These patterns are often attributed to passive loss from factors such as thymic atrophy and cumulative immune exposures but such processes fail to explain the systematic variation observed across populations. Here we challenge this view by analyzing TCR{beta} repertoires from[~] 30, 000 individuals showing that TCR diversity is almost entirely determined by repertoire size and the frequency of the 1,000 most abundant clones. These two intrinsic features of the repertoire explain 96% of the variance in TCR diversity, capturing its dependence on age and sex and defining a robust relationship that holds even under strong immune perturbations such as Cytomegalovirus infection. This relationship arises because the frequency of abundant clones captures a repertoire-wide pattern of coordinated clonal expansion--termed intrinsic clonality--which may be a fundamental, previously unrecognized property of the immune system. We propose that TCR diversity emerges as a system-level property mediated by repertoire size and intrinsic clonality, both of which are likely homeostatically regulated. These findings offer a new conceptual framework for understanding TCR diversity within immune homeostasis which may guide therapies aimed at restoring immune function.

immunology↗

Antigen-driven expansion of public clonal T cell populations in inflammatory bowel diseases

BackgroundInflammatory Bowel Diseases (IBDs), including Crohns disease (CD) and ulcerative colitis (UC), are known to involve shifts in the T-cell repertoires of affected individuals. These include a reduction in regulatory T cells in both diseases, increase in TNF production in CD, expansion of an unconventional T-cell population in CD, and clonal expansion of abundant T-cell populations in CD mucosal tissue. There are also differential HLA risk and protective alleles between CD and UC, implying CD- and UC-specific repertoire changes that have not yet been identified. MethodsWe performed ImmunoSequencing on blood samples from 3,853 CD cases, 1,803 UC cases, and 5,596 healthy controls. For each sample we imputed HLA type and cytomegalovirus (CMV) infection status based on public T-cell receptor {beta} (TCRB) usage and identified public TCRBs enriched in CD or UC cases. FindingsWe determine that there is more expansion across clonotypes in CD, but not UC, compared with healthy controls. We also identify novel interactive effects of HLA-DQ heterodimers with CD and UC risk. Strikingly, from blood we identify public TCRBs specifically expanded in CD or UC. These sequences are more abundant in intestinal mucosal samples, form groups of similar CDR3 sequences, and can be associated to specific HLA alleles. Although the prevalence of these sequences is higher in ileal and ileocolonic CD than colonic CD or UC, the TCRB sequences themselves are shared across CD and not between CD and UC. InterpretationThere are peptide antigens that commonly evoke immune reactions in IBD cases and rarely in non-IBD controls. These antigens differ between CD and UC. CD, particularly ileal CD, also seems to involve more substantial changes in clonal population structure than UC, compared to healthy controls.

immunology↗

Large-scale statistical mapping of T-cell receptor β sequences to Human Leukocyte Antigens

T-cell receptors (TCRs) interacting with peptides presented by human leukocyte antigens (HLAs) are the foundation of the adaptive immune system but population-level analysis of TCR-HLA interactions is lacking. Here we statistically associate[~] 106 public TCRs to specific HLAs using the TCR{beta} repertoires sampled from 4,144 HLA-genotyped subjects. The TCRs we associate are specific to unique HLA allotypes, not allelic groups, and to the paired -{beta} heterodimer of class II HLAs though exceptions are observed. This specificity permits highly accurate imputation of 248 class I and II HLAs from the TCR{beta} repertoire. Notably, 45 HLA-DP and -DQ heterodimers lack associated TCRs because they likely arise from non-functional trans-complementation. The public class I and II HLA-associated TCRs we identify are primarily expressed on CD8+ and CD4+ memory T cells, respectively, which are responding to various common antigens. Our results recapitulate fundamental biology, provide insights into the functionality of HLAs and demonstrate the power and potential of population-level TCR repertoire sequencing.

immunology↗

Seq2MAIT: A Novel Deep Learning Framework for Identifying Mucosal Associated Invariant T (MAIT) Cells

Mucosal-associated invariant T (MAIT) cells are a group of unconventional T cells that mainly recognize bacterial vitamin B metabolites presented on MHC-related protein 1 (MR1). MAIT cells have been shown to play an important role in controlling bacterial infection and in responding to viral infections. Furthermore, MAIT cells have been implicated in different chronic inflammatory diseases such as inflammatory bowel disease and multiple sclerosis. Despite their involvement in different physiological and pathological processes, a deeper understanding of MAIT cells is still lacking. Arguably, this can be attributed to the difficulty of quantifying and measuring MAIT cells in different biological samples which is commonly done using flow cytometry-based methods and single-cell-based RNA sequencing techniques. These methods mostly require fresh samples which are difficult to obtain, especially from tissues, have low to medium throughput, and are costly and labor-intensive. To address these limitations, we developed sequence-to-MAIT (Seq2MAIT) which is a transformer-based deep neural network capable of identifying MAIT cells in bulk TCR-sequencing datasets, enabling the quantification of MAIT cells from any biological materials where human DNA is available. Benchmarking Seq2MAIT across different test datasets showed an average area-under-the-receiver-operator-curve (AU[ROC]) >0.80. In conclusion, Seq2MAIT is a novel, economical, and scalable method for identifying and quantifying MAIT cells in virtually any biological sample.

bioinformatics↗

Perturbations of the T-cell immune repertoire in kidney transplant rejection

In this cross-sectional and longitudinal analysis of mapping the T-cell repertoire in kidney transplant recipients, we have investigated and validated T-cell clonality, immune repertoire chronology at rejection, and contemporaneous allograft biopsy quantitative tissue injury, to better understand the pathobiology of acute T cell and antibody-mediated kidney transplant rejection. To follow the dynamic evolution of T-cell repertoire changes before and after engraftment and during biopsy-confirmed acute rejection, we sequenced 323 peripheral blood samples from 200 unique kidney transplant recipients, with (n=100) and without (n=100) biopsyconfirmed acute rejection. The results of these studies highlight, for the first time, that patients who develop acute allograft rejection, have lower (p=0.01) T cell fraction even before transplantation, followed by its rise after transplantation and at the time of acute rejection accompanied by high TCR repertoire turnover (p=0.004). Acute rejection episodes occurring after the first 6 months post-transplantation, and those with a component of antibody-mediated rejection, had the highest turnover; p=0.0016) of their TCRs. In conclusion, further prospective validation studies are needed to evaluate the clinical utility of peripheral blood TCR analysis for both pre- and post-transplant immune risk assessment and prediction of different mechanisms of graft rejection.

immunology↗