Trial reportJournal of immunology (Baltimore, Md. : 1950)2011
Increased T cell proliferative responses to islet antigens identify clinical responders to anti-CD20 monoclonal antibody (rituximab) therapy in type 1 diabetes.
Trial report in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 83 citations in OpenAlex.
- Liraglutide and Βeta-Cell Function in Young Adults With Long-Standing Type 1 Diabetes and Residual C-Peptide: A Blinded, Randomized Controlled Trial.Diabetes, obesity & metabolism · 2026Trial
- Trial
- Intralymphatic glutamic acid decarboxylase administration in type 1 diabetes patients induced a distinctive early immune response in patients with DR3DQ2 haplotype.Frontiers in immunology · 2023Trial
- Elevated T cell levels in peripheral blood predict poor clinical response following rituximab treatment in new-onset type 1 diabetes.Genes and immunity · 2019Trial
- Trial
- Trial
- Effect of abatacept on immunogenicity of vaccines in individuals with type 1 diabetes.Vaccine · 2013Trial
- Reactivation of latent viruses in individuals receiving rituximab for new onset type 1 diabetes.Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology · 2013Trial
- Beta cell glucose sensitivity identifies clinical response to disease-modifying therapies initiated at stage 3 type 1 diabetes onset.Diabetologia · 2026Article
- New and emerging therapies in type 1 diabetes mellitus.The Journal of clinical investigation · 2026Review
- Are We Ready With Prevention for Type 1 Diabetes?Diabetes/metabolism research and reviews · 2025Review
- Activated polyreactive B cells are clonally expanded in autoantibody positive and patients with recent-onset type 1 diabetes.Cell reports · 2025Article
- Immunotherapies for prevention and treatment of type 1 diabetes.Immunotherapy · 2025Review
- Current perspectives and the future of disease-modifying therapies in type 1 diabetes.World journal of diabetes · 2025Article
- Pre-Type 1 Diabetes in Adolescents and Teens: Screening, Nutritional Interventions, Beta-Cell Preservation, and Psychosocial Impacts.Journal of clinical medicine · 2025Review
- Immunotherapy in type 1 diabetes: Novel pathway to the future ahead.World journal of diabetes · 2024Article
- Islet-antigen reactive B cells display a unique phenotype and BCR repertoire in autoantibody positive and recent-onset type 1 diabetes patients.bioRxiv : the preprint server for biology · 2024Article
- The immunology of type 1 diabetes.Nature reviews. Immunology · 2024Review
- Factors Governing B Cell Recognition of Autoantigen and Function in Type 1 Diabetes.Antibodies (Basel, Switzerland) · 2024Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
Type 1 diabetes mellitus is believed to be due to the autoimmune destruction of β-cells by T lymphocytes, but a single course of rituximab, a monoclonal anti-CD20 B lymphocyte Ab, can attenuate C-peptide loss over the first year of disease. The effects of B cell depletion on disease-associated T cell responses have not been studied. We compare changes in lymphocyte subsets, T cell proliferative responses to disease-associated target Ags, and C-peptide levels of participants who did (responders) or did not (nonresponders) show signs of β-cell preservation 1 y after rituximab therapy in a placebo-controlled TrialNet trial. Rituximab decreased B lymphocyte levels after four weekly doses of mAb. T cell proliferative responses to diabetes-associated Ags were present at baseline in 75% of anti-CD20- and 82% of placebo-treated subjects and were not different over time. However, in rituximab-treated subjects with significant C-peptide preservation at 6 mo (58%), the proliferative responses to diabetes-associated total (p = 0.032), islet-specific (p = 0.048), and neuronal autoantigens (p = 0.005) increased over the 12-mo observation period. This relationship was not seen in placebo-treated patients. We conclude that in patients with type 1 diabetes mellitus, anti-B cell mAb causes increased proliferative responses to diabetes Ags and attenuated β-cell loss. The way in which these responses affect the disease course remains unknown.
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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.