ArticleClinical immunology (Orlando, Fla.)2009
T cell receptor signaling induced by an analog peptide of type II collagen requires activation of Syk.
Article in Clinical immunology (Orlando, Fla.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 15 citations in OpenAlex.
- Kinase Inhibition as Treatment for Acute and Chronic Graft-Frontiers in immunology · 2021Review
- Peptide-Based Vaccination Therapy for Rheumatic Diseases.Journal of immunology research · 2020Review
- The role of Syk in peripheral T cells.Clinical immunology (Orlando, Fla.) · 2018Article
- Characterization of the Syk-Dependent T Cell Signaling Response to an Altered Peptide.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Peptide ligand structure and I-Aq binding avidity influence T cell signaling pathway utilization.Clinical immunology (Orlando, Fla.) · 2015Article
- Spleen tyrosine kinase (Syk) is a potent target for GvHD prevention at different cellular levels.Leukemia · 2012Article
- Molecular basis for T cell response induced by altered peptide ligand of type II collagen.The Journal of biological chemistry · 2012Article
- Immune-regulatory mechanisms in systemic autoimmune and rheumatic diseases.Clinical & developmental immunology · 2012Review
- T cells stimulated with an analog peptide of type II collagen require the Fc receptor γ-chain to secrete interleukin-4 and suppress autoimmune arthritis in mice.Arthritis and rheumatism · 2011Article
- Design of glycopeptides used to investigate class II MHC binding and T-cell responses associated with autoimmune arthritis.PloS one · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
We have previously described an analog peptide of type II collagen (CII) that can suppress collagen-induced arthritis (CIA). This analog peptide represents CII(245-270), the immunodominant epitope of CII, but with substitutions at 260, 261, and 263 - CII(245-270) (A(260), B(261), and N(263)) (A9). To elucidate the mechanisms responsible for suppression, we used mice transgenic for a collagen-specific T cell receptor (TCR). When we found that APCs pulsed with A9 failed to induce T cell phosphorylation of TCR-zeta and ZAP-70, we explored alternative signaling pathways. We determined that A9 instead induced phosphorylation of spleen tyrosine kinase (Syk). The importance of Syk was confirmed by the use of chemical Syk inhibitors, which blocked both cytokine secretion and activation of GATA-3 mediated by peptide A9. In summary, T cells use an alternative pathway in response to A9 that involves Syk. This novel T cell pathway may represent an important means for altering T cell phenotypes.
Indexed as
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.