Bibliographic record
Abstract
PURPOSE OF REVIEW: T cells are central to most inflammatory disorders of the intestine, particularly Celiac disease, graft vs. host disease, Crohn disease, and ulcerative colitis. The mechanisms by which T cells contribute to mucosal damage in these disorders have been explored using both in vitro and in vivo models. This review will highlight recent studies directed at understanding the mechanisms by which T cells are involved in the induction of mucosal damage. RECENT FINDINGS: The recent studies of in vivo T-cell activation using monoclonal anti-CD3 antibody have shown that a number of cytotoxic T-cell pathways are required and involved in the induction of mucosal damage and in particular in the induction of epithelial cell apoptosis. These include the Fas/FasL and perforin pathways. Other mediators of T-cell-induced cytotoxicity, such as TNFalpha and IFNgamma may contribute to mucosal damage but are not required for the induction of mucosal damage in vivo. In addition, several studies have tried to identify the role of regulatory mucosal T cells and the physiologically relevant triggers for T-cell-induced mucosal damage. SUMMARY: It is now clear that there are significant redundancies in the mechanisms that lead to immune-mediated mucosal damage and that the mechanisms that operate in vivo may not be predicted by in vitro experiments. These investigations are improving our understanding of the pathogenesis of immune-mediated enteropathies and will hopefully lead to new approaches to the management of these disorders.
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 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 | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 0.001 |
| Insufficient payload (model declined to judge) | 0.004 | 0.002 |
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".