Bibliographic record
Abstract
Abstract Two of the main challenges that eukaryotic multicellular organisms faced during evolution were to cope with invading microorganisms and to eliminate infected cells. The immune system evolved to handle both tasks. Intertwined with immunity is programmed cell death that tailors the immune response and provides an effective way to remove infected cells. Caspases, effectors of inflammation and programmed cell death cascades, are perfectly suited to regulate the host response to invaders and injury. Their activity as inflammatory and killer proteases is regulated by direct binding to sensors of pathogens or danger, they can be modified following activation of signalling cascades by feedback mechanisms to terminate the inflammatory response and control cell survival, and they associate with coactivators and corepressors whose expression is closely linked to the needs of the cell. Key concepts Cell death and innate immunity are ancient evolutionarily conserved processes that utilize a number of related effectors and parallel signal transduction mechanisms. Innate immunity provides first line defences against pathogens and acts as a sentinel that primes adaptive immunity. Innate immunity depends on evolutionarily conserved germline‐encoded pattern recognition receptors (PRRs) that ‘sense’ pathogen‐associated molecular patterns (PAMPs) and ‘danger’ signals. The role of caspases in innate immunity is conserved through evolution. Caspase‐1, the prototypical member of the inflammatory caspase subfamily, contributes to host defence through different interrelated mechanisms, notably cell repair, inflammation and cell death. Caspase‐1 activity is necessary for host resistance to pathogens; however, when deregulated, it is at the basis of multiple inflammatory diseases. Inflammatory caspases are activated in NLR‐scaffolded multiprotein complexes termed ‘inflammasomes’ that are reminiscent of the apoptosome. Caspase‐12, an inflammatory caspase related to caspase‐1, is an endogenous inhibitor of the inflammasome. Apoptosis tailors adaptive immunity. Mutations in Casp‐8 and Casp‐10 cause autoimmune lymphoproliferative syndrome (ALPS). Excessive apoptotic caspase activity contributes to the pathogenesis of inflammatory diseases such as severe sepsis.
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot 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.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.000 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.002 | 0.001 |
| Open science | 0.000 | 0.001 |
| Research integrity | 0.002 | 0.003 |
| Insufficient payload (model declined to judge) | 0.005 | 0.001 |
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.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
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".