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Record W2951065579 · doi:10.82308/35742

The role of b2-glycoprotein i-reactive t cells in the development of systemic lupus erythematosus

2019· article· en· W2951065579 on OpenAlexfundno aff
David Salem

Bibliographic record

VenueeScholarship@McGill (McGill) · 2019
Typearticle
Languageen
FieldMedicine
TopicSystemic Lupus Erythematosus Research
Canadian institutionsnot available
FundersFonds de Recherche du Québec - SantéCanadian Institutes of Health ResearchMcGill University Health CentreUniversity of Illinois at Urbana-ChampaignMcGill University
KeywordsEpitopeAutoantibodyImmunologyAntigenBiologyImmune systemT cellAntibody

Abstract

fetched live from OpenAlex

This thesis examines the role of β2-glycoprotein I (β2GPI)-reactive T cells in the development of systemic lupus erythematosus (SLE). SLE is a prototypic model for B cell epitope spread in autoimmunity. Autoantibodies to numerous molecularly distinct self-antigens emerge in a sequential manner over several years, leading to disease manifestations. Among the earliest autoantibodies to appear are those targeting phospholipids and phospholipid-binding proteins, particularly β2-glycoprotein I (β2GPI). Our laboratory has developed a model of SLE in which mice immunized with β2GPI and lipopolysaccharide (LPS) display a remarkably similar pattern of autoantibody emergence to that seen in human SLE, as well as SLE-like kidney disease. Here we use this model to investigate whether epitope spread to SLE autoantibodies is associated with a unique or limited β2GPI-reactive T cell response. We ask whether MHC class II haplotype, and its associated T cell epitope restriction, impacts epitope spread to SLE autoantibodies. Furthermore, we investigate the origin of β2GPI-reactive T cells initiating this epitope spread. We hypothesize that binding of β2GPI to necroptotic cells presents the immune system with a "scaffold" of cellular self-antigens in a pro-inflammatory and immunogenic context, leading to a robust β2GPI-reactive T cell response. Splenocytes from β2GPI/LPS-immunized mice with different MHC class II haplotypes were used to determine β2GPI-reactive T cell epitopes, using a peptide library spanning the entire sequence of human β2GPI. One β2GPI-reactive T cell epitope (LYRDTAVFECLPQHAMFG) in Domain III appeared to be a dominant epitope, since it was recognized in β2GPI/LPS-immunized mice with different MHC class II haplotypes, as well as in SLE-prone MRL/lpr mice. We next showed that β2GPI binds to necroptotic, as well as apoptotic, L929 cells but that necroptotic, not apoptotic, cells enhance pro-inflammatory cytokine (TNF-α) secretion by activated macrophages and dendritic cells in vitro. Necroptotic cells promoted MHC class II and costimulatory molecule expression in immature dendritic cells, leading to an enhanced CD4 T cell response to β2GPI in vitro. Finally, we show that mice deficient in Ripk3 (receptor-interacting serine/threonine-protein kinase 3), and hence necroptosis, show poor induction of SLE. In summary, we propose that factors enabling a β2GPI-reactive T cell response may predispose individuals to the development of SLE autoantibodies independent of their MHC class II haplotype. Furthermore, our findings suggest that necroptotic cells provide both self-antigens and pro-inflammatory signals that may be sufficient to overcome immune tolerance and induce SLE.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.003

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0010.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.014
GPT teacher head0.247
Teacher spread0.233 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations0
Published2019
Admission routes1
Has abstractyes

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