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Rai, B.

Publications and source records attributed to Rai, B..

9 recordsLinked to original sources

Limitations of general protein language models and public TCRpMHC data in training specificity prediction models

T cell receptor (TCR) specificity prediction is critical for understanding adaptive immunity and for enabling the development of therapeutic interventions. Current machine learning models for predicting TCR-peptide-MHC interactions perform poorly, despite large efforts by many groups and advances in protein language models. This work identifies and addresses the fundamental issues that might be hindering progress in this field, focusing on current approaches for constructing training and validation sets, particularly on the strategies used by commonly used methods, which generate negative data either by shuffling TCRs between epitopes or by pairing epitopes with TCRs from background datasets of healthy donors. Here, we visualize and quantify the overlap between positive and generated negative TCR sets produced by both strategies using a range of sequence embedding approaches, including simple encodings (one-hot and BLOSUM62), general protein language models (ESM-2 and ProtGPT2), and a TCR-specific embedding model (TCR-BERT). Using paired {beta}TCR data from VDJdb for two well-studied epitopes (GILGFVFTL and KLGGALQAK), we train Random Forest classifiers on each embedding representation and evaluate their ability to distinguish positive from negative data examples. We find that general sequence embedding methods struggle to differentiate between positive and negative TCRs. We further show that the choice of negative data generation method significantly impacts classifier performance. Our findings highlight fundamental limitations in current TCR specificity training data and general protein language models, and underscore the need for TCR-specific embeddings, experimentally validated negative datasets, transparent reporting of negative data construction, and epitope-specific modeling approaches.

bioinformatics↗

Oral L-arginine cures arginase 1-dependent chronic cutaneous leishmaniasis by redirecting the T helper cell response

Leishmania (L.) mexicana-induced cutaneous leishmaniasis (CL) is a neglected tropical disease characterized by localized chronic ulcers (LCL) and, in rare cases, by disseminated skin lesions (DCL). The therapeutic options for CL are currently limited, and the immune dysregulation leading to chronicity of disease is poorly understood. Here, we identified interleukin (IL)-10-dependent upregulation of arginase 1 (ARG1) in cutaneous CX3CR1+ myeloid cells as central immunometabolic determinant of chronic CL in L. mexicana-infected C57BL/6 wild-type (WT) mice. Deletion of Arg1 in myeloid cells (Arg1{Delta}Cx3cr1) enabled parasite control and clinical healing. Single-cell RNA sequencing revealed that ARG1, together with interferon-{gamma} produced by T-helper 1 (Th1) cells, caused pathologic differentiation of Ly6Chigh monocytes into inflammatory macrophages (iMACs) that simultaneously expressed ARG1, nitric oxide synthase type 2 (NOS2) and the chemokines CXCL9/10. These Arg1+Nos2+Cxcl9/10+iMACs induced a lasting depletion of L-arginine in the skin, served as parasite niche, and maintained a self-perpetuating cycle of host cell recruitment. In Arg1{Delta}Cx3cr1 mice, the ARG1+NOS2+ host cell niche for the parasite was diminished. Prophylactic or therapeutic oral L-arginine supplementation restored tissue arginine levels, reduced parasite burden, and prevented or resolved chronic disease. L-arginine-treated mice showed enhanced T cell expansion and Th1 differentiation, remained free of clinical relapses, and were resistant to reinfection. As skin lesion biopsies from L. mexicana-infected LCL and DCL patients demonstrated a similar pattern of Th1/Th2 cytokine, Arg1 and Nos2 mRNA expression as seen in mice, we suggest metabolic reprogramming by oral L-arginine as a promising and easy-to-apply host-directed therapy for human L. mexicana CL. ONE SENTENCE SUMMARYArginase 1-mediated arginine depletion accounts for chronic cutaneous leishmaniasis, which can be prevented and even cured by oral L-arginine therapy.

immunology↗

The metabolic program of inflammatory eosinophils accounts for chronic parasite-induced skin-disease

Eosinophils exert antimicrobial, cytotoxic and immunoregulatory effects, but their function in cutaneous tissue still remains poorly understood. Here, we used a mouse model of chronic cutaneous leishmaniasis caused by the protozoan parasite Leishmania (L.) mexicana to investigate the function and transcriptomic signature of eosinophils in the skin. In C57BL/6 wild-type mice, L. mexicana infection induced local and systemic eosinophilia that was dependent on type 2 innate lymphoid cells and interleukin-5. Genetic and pharmacological depletion of eosinophils led to complete clinical resolution of disease, which was accompanied by a more pronounced Th1 and M1-like macrophage response. Bioinformatic analyses revealed a novel inflammatory and tissue-specific transcriptional trajectory in skin-infiltrating eosinophils. Skin-imprinted eosinophils strongly expressed the high-affinity glucose transporter 3 (Slc2a3), deprived the environment of glucose and directly impeded the function of Th1 cells. Together, our results demonstrate that disease progression and chronicity of L. mexicana infection is caused by inflammatory eosinophils and linked to their metabolic program. Short SummaryThe authors describe that depletion of eosinophils prevents chronic cutaneous disease caused by Leishmania mexicana. They identify a novel, tissue-specific transcriptomic profile of inflammatory skin eosinophils and demonstrate that skin-imprinted eosinophils show strong glucose uptake and directly repress Th1 responses. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=173 SRC="FIGDIR/small/640104v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@3ecd3org.highwire.dtl.DTLVardef@1b1283forg.highwire.dtl.DTLVardef@1c941fdorg.highwire.dtl.DTLVardef@b7c39_HPS_FORMAT_FIGEXP M_FIG C_FIG KEY POINTSO_LIEosinophil accumulation precedes the development of chronic cutaneous leishmaniasis C_LIO_LIEosinophil depletion or IL-5 neutralization lead to clinical cure of the disease C_LIO_LIL. mexicana infection elicits a unique transcriptomic signature of skin eosinophils C_LIO_LISkin eosinophils show a marked uptake of glucose and directly repress Th1 responses C_LI

immunology↗

HLAIIPred: Cross-Attention Mechanism for Modeling the Interaction of HLA Class II Molecules with Peptides

We introduce HLAIIPred, a deep learning model to predict peptides presented by class II human leukocyte antigens (HLAII) on the surface of antigen presenting cells. HLAIIPred is trained using a Transformer-based neural network and a dataset comprising of HLAII-presented peptides identified by mass spectrometry. In addition to predicting peptide presentation, the model can also provide important insights into peptide-HLAII interactions by identifying core peptide residues that form such interactions. We evaluate the performance of HLAIIPred on three different tasks, peptide presentation in monoallelic samples, immunogenicity prediction of therapeutic antibodies, and neoantigen prioritization for cancer immunotherapy. Additionally, we created a dataset of biotherapeutics HLAII peptides presented by human dendritic cells. This data is used to develop screening strategies to predict the unwanted immunogenic segments of therapeutic antibodies by HLAII presentation models. HLAIIPred demonstrates superior or equivalent performance when compared to the latest models across all evaluated benchmark datasets. We achieve a 16% increase in prediction of presented peptides compared to the second-best model on a set of unseen peptides presented by less frequent alleles. The model improves clinical immunogenicity prediction, identifies epitopes in therapeutic antibodies and prioritize neoantigens with high accuracy. HIGHLIGHTS* We developed a deep learning model to address the shortcomings of existing models for the prediction of peptides presented by HLAII molecules. * The model is end-to-end and context-free, requiring only a peptide sequence and available HLAII alleles as input. * HLAIIPred outperforms the state-of-the-art models on multiple benchmark datasets. * The model is able to predict the core residues of peptides that interact with HLAIIs. * We created experimental data and developed screening strategies to accurately predict the immunogenic hotspots in therapeutic antibodies.

bioinformatics↗

Altered Expression of microRNAs Implicated in Hematopoietic Dysfunction in the Extracellular Vesicles of Bone Marrow-Mesenchymal Stromal Cells in Aplastic Anemia

Recently, we have reported that extracellular vesicles (EVs) from the bone marrow mesenchymal stromal cells (BM-MSC) of aplastic anemia (AA) patients inhibit hematopoietic stem and progenitor cell (HSPC) proliferative and colony-forming ability and promote apoptosis. One mechanism by which AA BM-MSC EVs might contribute to these altered HSPC functions is through microRNAs (miRNAs) encapsulated in EVs. However, little is known about the role of BM-MSC EVs derived miRNAs in regulating HSPC functions in AA. Therefore, we performed miRNA profiling of EVs from BM-MSC of AA (n=6) and normal controls (NC) (n=6), to identify differentially expressed miRNAs carried in AA BM-MSC EVs. DEseq2 analysis identified 34 significantly altered mature miRNAs in AA BM-MSC EVs. Analysis of transcriptome dataset of AA HSPC genes identified that 235 differentially expressed HSPC genes were targeted by these 34 EV miRNAs. The pathway enrichment analysis of 235 HSPC genes revealed their involvement in pathways associated with cell cycle, proliferation, apoptosis, and hematopoiesis regulation, thus highlighting that AA BM-MSC EV miRNAs could potentially contribute to impaired HSPC functions in AA.

molecular biology↗

Bioenergetic mapping of 'healthy microbiomes' via compound processing potential imprinted in gut and soil metagenomes

Despite mounting evidence of their importance in human health and ecosystem functioning, the definition and measurement of healthy microbiomes remain unclear. More advanced knowledge exists on health associations for compounds used or produced by microbes. Environmental microbiome exposures (especially via soils) also help shape, and may supplement, the functional capacity of human microbiomes. Given the synchronous interaction between microbes, their feedstocks, and micro-environments, with functional genes facilitating chemical transformations, there exists an intriguing opportunity to examine microbiomes in terms of their capacity to process compounds relevant to human health. Here we integrate functional genomics and biochemistry frameworks to derive new quantitative measures of the potential for human gut and environmental soil metagenomes to process major compound classes (e.g., lipids, carbohydrates) and selected biomolecules (e.g., vitamins, short-chain fatty acids) linked to human health. Metagenome functional potential profile data were translated into a universal compound mapping landscape based on bioenergetic van Krevelen mapping of function-level meta-compounds and corresponding functional relative abundances, reflecting imprinted genetic capacity of microbiomes to metabolize an array of different compounds. We show that measures of compound processing potential associated with human health and disease (examining atherosclerotic cardiovascular disease, colorectal cancer, type 2 diabetes and anxious-depressive behavior case studies), and displayed seemingly predictable shifts along gradients of ecological disturbance in plant-soil ecosystems (three case studies). Ecosystem quality explained 60-92% of variation in soil metagenome compound processing potential measures in a post-mining restoration case study dataset. With growing knowledge of the varying proficiency of environmental microbiota to process human health associated compounds, we might design environmental interventions or nature prescriptions to modulate our exposures, thereby advancing microbiota-oriented approaches to human health. Compound processing potential offers a simplified, integrative approach for applying metagenomics in ongoing efforts to understand and quantify the role and linkages of microbiota in environmental- and human-health.

bioinformatics↗

RVE based Finite Element Modelling of the Contact Mechanics Between Skin and Indenter

The nature of contact between human skin and external object (such as medical device, personal care device, fabric and so on) significantly influences the tactile perception and/or the functionality of the object. The contact mechanics depends strongly on the indenter properties and the mechanical properties of skin. Further, the topmost layer i.e., stratum corneum plays the most important role in tactile perception. In this study we use a representative volume element (RVE) based FEM model including the four layers of skin - stratum corneum, epidermis, dermis, and hypodermis - to simulate the contact mechanics between skin and a spherical indenter. The RVE model captures the mechanical properties of the microscopic constituents of the stratum corneum, which is the topmost layer of skin. We found that the RVE model can be used to simulate a variety of stratum corneum conditions (for example, dry and wet stratum corneum) and compositions. Using the RVE model in conjunction with an FEM model, we compute the frictional stress between skin and an indenter, as a function of stratum corneum microstructure, indentation depth, and local coefficient of friction. Both, the RVE model and the contact mechanics model predictions show good qualitative agreement with experimental findings in literature. Such studies will be very useful in in-silico design and optimization of devices that interact with skin. The current framework gives control over several parameters like skin microstructure, indenter or skin geometry and hence can be used to augment/substitute experimental testing.

biophysics↗

Elucidating Collective Translocation of Nanoparticles Across the Skin Lipid Barrier: A Molecular Dynamics Study

The top layer of skin, the stratum corneum, provides a formidable barrier to the skin. Nanoparticles are utilized and further explored for personal and health care applications related to the skin. In past years several researchers have studied the translocation and permeation of nanoparticles of various shapes, sizes, and surface chemistry through the cell membranes. Most of these studies focused on a single nanoparticle and a simple bilayer system, whereas skin has a highly complex lipid membrane architecture. Moreover, it is highly unlikely that a nanoparticle formulation applied on the skin will not have multiple nanoparticle-nanoparticle and skin-nanoparticle interactions. In this study, we have utilized coarse-grained MARTINI molecular dynamics simulations to assess the interactions of two types (bare and dodecane-thiol coated) of nanoparticles with two models (single bilayer and double bilayer) of skin lipid membranes. The nanoparticles were found to be partitioned from the water layer to the lipid membrane as an individual entity as well as in the cluster form. It was discovered that each nanoparticle reached the interior of both single bilayer and double bilayer membrane irrespective of nanoparticle type and concentration, though coated particles were observed to efficiently traverse across bilayer when compared with bare particles. The coated nanoparticles also created a single large cluster inside the membrane, whereas bare nanoparticles were found in small clusters. Both the nanoparticles exhibited preferential interactions with cholesterol molecules present in the lipid membrane as compared to other lipid components of the membrane. We have also observed that the single membrane model exhibited unrealistic instability at moderate to the higher concentration of nanoparticles, and hence for translocation study, at minimum double bilayer model should be employed.

biophysics↗

Copper dependent ERK1/2 phosphorylation is essential for the viability of neurons and not glia

Intracellular Copper [Cu(I)] has been hypothesized to play role in the differentiation of the neurons. This necessitates understanding the role of Cu(I) not only in the neurons but also in the glia considering their anatomical proximity, contribution towards ion homeostasis, neuronal physiology, and neurodegeneration. In this study we did a systematic investigation of the changes in the cellular copper homeostasis during neuronal and glial differentiation and the pathways triggered by them. Our study demonstrates increased mRNA for the plasma membrane copper transporter CTR1 leading to an increased Cu(I) during neuronal (PC-12) differentiation. ATP7A is retained in the Trans Golgi Network (TGN) despite high Cu(I) demonstrating its utilization in triggering the pathways towards the neuronal differentiation. One of these pathways is ERK1/2 phosphorylation accompanying the differentiation of both PC-12 and human fetal brain derived neuronal progenitor cells. The study demonstrates that the ERK1/2 phosphorylation is essential for the viability of the neurons. In contrast, differentiated C-6 (glia) cells contain low intracellular copper and significant downregulation of the ERK1/2 phosphorylation. Interestingly ATP7A shows vesicular localization despite the low copper in the glia. In addition to the TGN in the perinuclear region, ATP7A localizes into RAB11 positive recycling endosomes in the glial neurites, not observed in the neurons. Our study demonstrates role of the copper dependent ERK1/2 phosphorylation in the neuronal differentiation. Whereas glial differentiation largely involves sequestration of Cu(I) into the endosomes potentially (i) for ready release to the neurons (ii) rendering cytosolic copper unavailable for pathways like the ERK1/2 activation.

cell biology↗