Publications by authors named "V Corrigall"
A homologue of binding immunoglobulin protein/BiP-IRL201805 alters the function of immune cells in pre-clinical in vivo and in vitro studies. The aim of the study was to select biomarkers that clearly delineate between RA patients who respond to IRL201805 and placebo patients and reveal the immunological mode of action of IRL201805 driving the extended pharmacodynamics observed in responding patients. Biomarkers that distinguished between responding patients and placebo patients included downregulation of serum interferon-γ and IL-1β; upregulation of anti-inflammatory mediators, serum soluble CTLA-4, and intracellular monocyte expression of IDO; and sustained increased CD39 expression on CD3CD4CD25 CD127 regulatory T cells.
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- Two major chaperones, calreticulin (CRT) and binding immunoglobulin protein (GRP78/BiP), have distinct immunoregulatory functions: CRT promotes inflammation and T cell activation, while GRP78/BiP induces anti-inflammatory responses and regulates immune balance.
- Endogenous CRT on cancer cells signals for their removal by immune cells, but infused CRT can hinder this process; conversely, low levels of BiP can indicate ER stress in tumors.
- Therapeutics targeting the surface relocation of these chaperones, such as enhancing CRT exposure or infusing GRP78/BiP analogs, are being explored in clinical trials to improve immune responses in diseases like cancer and rheumatoid arthritis.
Article Synopsis
- A study was conducted to evaluate the impact of a peptide sequence derived from Mycobacteria tuberculosis chaperonin 60.1, named IRL201104, on allergic lung inflammation in mice and guinea pigs.
- Pre-treatment with IRL201104 resulted in reduced eosinophil infiltration, cytokine release, and improved vascular permeability in guinea pigs, along with sustained anti-inflammatory effects for up to 20 days post-treatment.
- The peptide also increased expression of the anti-inflammatory molecule ubiquitin A20 and inhibited NF-κB activation, suggesting it could play a role in reducing allergic disease inflammation, particularly in asthma patients.
Objective: The association between inflammation and dysregulated bone remodeling is apparent in rheumatoid arthritis and is recapitulated in the human tumor necrosis factor transgenic (tg) mouse model. We investigated whether extracellular binding immunoglobulin protein (BiP) would protect the tg mouse from both inflammatory arthritis as well as extensive systemic bone loss and whether BiP had direct antiosteoclast properties in vitro.
Methods: tg mice received a single intraperitoneal administration of BiP at onset of arthritis.
Article Synopsis
- The PD-1 receptor is crucial for regulating T cell activation, and this study investigates how inflammation affects PD-1's suppressive role on T cells, particularly in rheumatoid arthritis (RA) and psoriatic arthritis (PsA).
- Analysis revealed a higher percentage of PD-1-expressing CD4 and CD8 T cells in synovial fluid from RA and PsA patients compared to their peripheral blood.
- Inflammation-related cytokines significantly diminished PD-1's inhibitory effects on healthy CD4 T cells, indicating that RA and PsA T cells may be less responsive to PD-1 suppression due to the inflammatory environment, which also contains increased levels of soluble PD-1.