ReviewClinical & developmental immunology2012
Coinhibitory molecules in autoimmune diseases.
Review in Clinical & developmental immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Review
- cTfh Cell Activation and Changes in BTLA and LAG-3 Expression Differentially Associate With Poor Pregnancy Outcome in Plasmodium falciparum Placental Malaria.Journal of immunology research · 2026Article
- Review
- Metformin attenuates V-domain Ig suppressor of T-cell activation through the aryl hydrocarbon receptor pathway in Melanoma: In Vivo and In Vitro Studies.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022Article
- The association ofFrontiers in immunology · 2022Article
- Article
- Lower Functional and Proportional Characteristics of Cord Blood Treg of Male Newborns Compared with Female Newborns.Biomedicines · 2021Article
- Abnormal Expression of BTLA and CTLA-4 Immune Checkpoint Molecules in Chronic Lymphocytic Leukemia Patients.Journal of immunology research · 2020Article
- New therapeutic targets for cancer: the interplay between immune and metabolic checkpoints and gut microbiota.Clinical and translational medicine · 2019Review
- Nocardiosis in Kidney Disease Patients under Immunosuppressive Therapy: Case Report and Literature Review.International journal of medical sciences · 2019Review
- Metformin Promotes Antitumor Immunity via Endoplasmic-Reticulum-Associated Degradation of PD-L1.Molecular cell · 2018Article
- Defective BTLA functionality is rescued by restoring lipid metabolism in lupus CD4+ T cells.JCI insight · 2018Article
- Article
- MUC1 Mucin: A Putative Regulatory (Checkpoint) Molecule of T Cells.Frontiers in immunology · 2018Review
- Molecular and Cellular Characterization of Human CD8 T Suppressor Cells.Frontiers in immunology · 2016Review
- Myeloid-derived suppressor cells impair alveolar macrophages through PD-1 receptor ligation during Pneumocystis pneumonia.Infection and immunity · 2015Article
- Tumor necrosis factor superfamily in innate immunity and inflammation.Cold Spring Harbor perspectives in biology · 2014Review
- Autoimmunity versus autoinflammation--friend or foe?Wiener medizinische Wochenschrift (1946) · 2014Review
- Restoring the balance: immunotherapeutic combinations for autoimmune disease.Disease models & mechanisms · 2014Review
- Cytotoxic-T-lymphocyte antigen 4 receptor signaling for lymphocyte adhesion is mediated by C3G and Rap1.Molecular and cellular biology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coinhibitory molecules such as CTLA-4, PD-1 and BTLA negatively regulate immune responses. Multiple studies indicate that the deficiency or mutation of coinhibitory molecules leads to the development of autoimmune diseases in mice and humans, indicating that the negative signals from coinhibitory molecules are crucial for the prevention of autoimmunity. In some conditions, the administration of decoy coinhibitory receptors (e.g., CTLA-4 Ig) or mAb against coinhibitory molecules suppresses the responses of self-reactive T cells in autoimmune diseases. Therefore, modulation of coinhibitory signals seems to be an attractive approach to induce tolerance in autoimmune diseases in humans where the disease-inducing self-antigens are not known. Particularly, administration of CTLA-4 Ig has shown great promise in animal models of autoimmune diseases and has been gaining increasing attention in clinical investigation in several autoimmune diseases in humans.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.