MétaCan
Menu
Back to cohort
Record W4414677407 · doi:10.3389/fimmu.2025.1506124

RIPK3 impacts antibody generation in an induced model of murine lupus through mechanisms other than necroptosis and antigen presentation

2025· article· en· W4414677407 on OpenAlexafffund
Céleste Pilon, Elena Lonina, Jerrold S. Levine, Sylvie Lesage, Joyce Rauch

Bibliographic record

VenueFrontiers in Immunology · 2025
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCell death mechanisms and regulation
Canadian institutionsUniversité de MontréalHôpital Maisonneuve-RosemontMcGill University Health Centre
FundersCanadian Institutes of Health Research
KeywordsNecroptosisAutoantibodySystemic lupus erythematosusAntibodyAntigenAutoimmunity

Abstract

fetched live from OpenAlex

Introduction Receptor-interacting protein kinase 3 (RIPK3) is a protein involved in cell death and inflammatory processes. The most recognized function of RIPK3 is the induction of necroptosis, an inflammatory type of cell death that is dependent on RIPK3 kinase activity. Deficiency in RIPK3-dependent pathways has been associated with protection from various inflammatory and autoimmune conditions. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the generation of autoantibodies to multiple intracellular antigens leading to multi-organ pathology. Little is known about the involvement of RIPK3-dependent pathways in SLE. We have previously shown that autoantibody generation in an induced model of murine lupus is impaired in RIPK3-deficient mice. The current study aimed to identify the RIPK3-dependent mechanisms that contribute to autoantibody generation in this induced model of murine lupus. Methods SLE was induced in C57BL/6 (wild type), RIPK3-/-, RIPK3K51A/K51A, and MLKL-/- mice by subcutaneous immunization with a mixture of β2-glycoprotein I and lipopolysaccharide in order to evaluate the contribution of RIPK3 and MLKL to autoantibody production in this model. Bone marrow chimeras were generated to investigate the impact of RIPK3 deficiency within the hematopoietic compartment. Antigen presentation assays assessed the impact of RIPK3 deficiency in antigen presenting cells on T cell activation in vitro. T cells were evaluated ex vivo by flow cytometry following the induction of SLE in wild type and RIPK3-dependent pathway-deficient mice. Results Generation of autoantibodies to SLE antigens following immunization with β2-glycoprotein I and lipopolysaccharide was found to be dependent on RIPK3 activity, but independent of MLKL (i.e., RIPK3-dependent necroptosis). Bone marrow chimeric experiments revealed that RIPK3 mediates autoantibody generation through both immune and non-immune compartments. RIPK3 deficiency within antigen presenting cells did not impact T cell activation in vitro. Moreover, early and late T cell activation ex vivo was not impaired in RIPK3-deficient mice following induction of murine lupus. Conclusion These results suggest that RIPK3 contributes to autoantibody generation in our induced model of murine lupus through an interplay of pathways that appear to be independent of necroptosis and antigen presentation.

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: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.008

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0010.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0010.002
Insufficient payload (model declined to judge)0.0020.001

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 head0.279
Teacher spread0.264 · 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 designBench or experimental
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

Citations1
Published2025
Admission routes2
Has abstractyes

Explore more

Same venueFrontiers in ImmunologySame topicCell death mechanisms and regulationFrench-language works237,207