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High-Dose Immunosuppression and Autologous Transplantation for Multiple Sclerosis (HALT MS) Study

ClinicalTrials.gov study NCT00288626. IPD Sharing: YES. Countries: 1. Publications: 11.

Mycophenolate Mofetil Immunosuppression Without/With Reduced Dose Calcineurin Inhibitor Long After Liver Transplantation

ClinicalTrials.gov study NCT00206076. IPD Sharing: Not stated. Countries: 1. Publications: 14.

Steroid-Free Versus Steroid-Based Immunosuppression in Pediatric Renal (Kidney) Transplantation

ClinicalTrials.gov study NCT00141037. IPD Sharing: YES. Countries: 1. Publications: 7.

Progression of Renal Interstitial Fibrosis / Tubular Atrophy (IF/TA) According to Epithelial-mesenchymal Transition (EMT) and Immunosuppressive Regimen (Everolimus Based Versus CNI Based) in de Novo R

ClinicalTrials.gov study NCT01079143. IPD Sharing: Not stated. Countries: 1. Publications: 1.

Belatacept Evaluation of Nephroprotection and Efficacy as First-line Immunosuppression (BENEFIT)

ClinicalTrials.gov study NCT00256750. IPD Sharing: Not stated. Countries: 21. Publications: 3.

closedIPD-NOFeb 2026View details →

Once Daily Immunosuppression Regimen

ClinicalTrials.gov study NCT03555448. IPD Sharing: NO. Countries: 1. Publications: 6.

Islet Transplantation in Type 1 Diabetics Using the Edmonton Protocol of Steroid Free Immunosuppression

ClinicalTrials.gov study NCT00133809. IPD Sharing: Not stated. Countries: 1. Publications: 1.

Open-Label Phase 2 Trial of a Steroid-Free, CNI-Free, Belatacept-Based Immunosuppressive Regimen

ClinicalTrials.gov study NCT01856257. IPD Sharing: YES. Countries: 1. Publications: 1.

Withdrawal of Immunosuppression in Pediatric Liver Transplant Recipients

ClinicalTrials.gov study NCT00320606. IPD Sharing: YES. Countries: 1. Publications: 4.

Safety Outcomes of Lower Immunosuppression Versus Traditional Immunosuppression in Heart Transplant Recipients

ClinicalTrials.gov study NCT00299221. IPD Sharing: Not stated. Countries: 1. Publications: 2.

publicAug 2023View details →

dryad36/100

Data from: Desmoplastic stroma restricts T cell extravasation and mediates immune exclusion and immunosuppression in solid tumors

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opencc-zeroMay 2020View details →

Low-dose alemtuzumab induction in a tailored immunosuppression protocol for sensitized kidney transplant recipients

Background: Induction therapy is crucial in kidney transplantation and constitutes an important cornerstone for long-term allograft survival. Alemtuzumab is a depleting CD52-specific antibody with T and B cell activity, leading to prolonged lymphocyte depletion for up to 12 months, with profound immunosuppression and an associated risk of serious infections. Current concepts aim to optimize dosing strategies to reduce side effects. Here we present data from an ongoing centre protocol consisting of low-dose alemtuzumab induction and tailored immunosuppression in sensitized patients undergoing kidney transplantation. Methods: 10-year results of the protocol were analysed. Low-dose alemtuzumab induction consisted of a single dose of 20mg intraoperatively, followed by tacrolimus and corticosteroids for initial immunosuppression, with mycophenolate mofetil suspended until a total lymphocyte count >5% or 200/µl was reached. Results: Between 01/2007 and 04/2017, 46 patients were treated in accordance with the protocol in 48 kidney transplantations. Median PRAmax was 43 [22-76; IQR] %; all patients had negative CDC-crossmatch prior to transplantation. Low-dose alemtuzumab was well tolerated. Median time to TLC recovery was 77 [62-127; IQR] d. Within a median follow-up of 3.3 [1.5-5.6; IQR] years, 12 (25%) patients developed BPAR, 10 of which were antibody-mediated (3 acute, 7 chronic ABMR). Death-censored 5-year allograft survival was 79.2%, with an excellent allograft function at the end of follow-up. There was no increased rate of infections, in particular viral infections. Conclusions: Our protocol, comprising low-dose alemtuzumab induction, initial suspension of mycophenolate mofetil and triple maintenance immunosuppression, provides excellent patient and allograft outcome in sensitized renal allograft recipients.

opencc-zeroJul 2020View details →

Data from: Hypothalamic circuitry underlying stress-induced insomnia and peripheral immunosuppression

The neural substrates of insomnia/hyperarousal induced by stress remain unknown. Here, we show that restraint stress leads to hyperarousal associated with strong activation of corticotropin-releasing hormone neurons in the paraventricular nucleus of hypothalamus (CRHPVN) and hypocretin neurons in the lateral hypothalamus (HcrtLH). CRHPVN neurons directly innervate HcrtLH neurons and optogenetic stimulation of LH-projecting CRHPVN neurons elicits hyperarousal. CRISPR-Cas9-mediated knockdown of the crh gene in CRHPVN neurons abolishes hyperarousal induced by stimulating LH-projecting CRHPVN neurons. Genetic ablation of Hcrt neurons or crh gene knockdown significantly counteracts restraint stress-induced hyperarousal. As stress is further associated with changes in immune function, we used single-cell mass cytometry by time of flight (CyTOF) to analyze peripheral blood and found extensive changes to immune cell distribution and functional responses during wakefulness upon optogenetic stimulation of CRHPVN neurons. Our findings suggest both central and peripheral systems are synergistically engaged in the response to stress via CRHPVN circuitry.

opencc-zeroAug 2020View details →

Aetiology and prognostic risk factors of mortality in pneumonia patients receiving glucocorticoids alone or glucocorticoids and other immunosuppressants: a retrospective cohort study

Objectives: Long-term use of high-dose glucocorticoids can lead to severe immunosuppression and increased risk of treatment-resistant pneumonia and mortality. We investigated the aetiology and prognostic risk factors of mortality in hospitalised patients who developed pneumonia while receiving glucocorticoid therapy alone or glucocorticoid and other immunosuppressant therapies. Design: Retrospective cohort study Setting: Six secondary and tertiary academic hospitals in China Participants: Patients receiving glucocorticoids who were hospitalised with pneumonia between 1st January 2013 and 31st December 2019. Main Outcomes: We analysed the prevalence of comorbidities, microbiology, antibiotic susceptibility patterns, 30-day and 90-day mortality rates, and prognostic risk factors. Results: A total of 716 patients were included, with pneumonia pathogens identified in 69.8% of patients. Significant morbidities occurred, including respiratory failure (50.8%), intensive care unit (ICU) transfer (40.8%), and mechanical ventilation (36%), with a 90-day mortality rate of 26.0%. Diagnosis of pneumonia occurred within 6 months of glucocorticoid initiation for 69.7% of patients with Cytomegalovirus (CMV) pneumonia and 79.0% of patients with Pneumocystis jirovecii pneumonia (PCP). Pathogens, including Pneumocystis, CMV, and multidrug-resistant bacteria, were identified more frequently in patients with persistent lymphocytopenia and high-dose glucocorticoid treatment (≥ 30 mg/day of prednisolone or equivalent within 30 days before admission). The 90-day mortality rate was significantly lower for non-CMV viral pneumonias than for PCP (P < 0.05), with a similar mortality rate as CMV pneumonias (24.2% vs 38.1% vs 27.4%, respectively).Cox regression analysis indicated <a name="_Hlk30339725"></a><a name="_Hlk31278800">several independent negative predictors for mortality in this patient population, including septic shock, respiratory failure, </a>persistent lymphocytopenia, interstitial lung disease, and high-dose glucocorticoid use. Conclusions: Patients who developed pneumonia while receiving glucocorticoid therapy experienced high rates of opportunistic infections, with significant morbidity and mortality. These findings should be carefully considered when determining treatment strategies for this patient population.

opencc-by-4.0Oct 2019View details →

Data and results for Cochrane systematic review and network meta-analysis on 'Induction immunosuppression in adults undergoing liver transplantation: a network meta-analysis'

This contains the data and the raw results for the Cochrane systematic review and network meta-analysis on Induction immunosuppression in adults undergoing liver transplantation: a network meta-analysis (<a href="https://doi.org/10.1002/14651858.CD013203">https://doi.org/10.1002/14651858.CD013203</a>). Please unzip the file and read the instructions before using the data.

opencc-by-4.0Sep 2024View details →

Single-cell RNA sequencing reveals immunosuppressive pathways associated with metastatic breast cancer

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opencc-zeroJun 2023View details →

Tim-3 regulates the immunosuppressive function of decidual MDSCs via the Fyn-STAT3-C/EBPβ pathway during Toxoplasma gondii infection

Myeloid-derived suppressor cells (MDSCs) play a key role in maintaining maternal-fetal tolerance for a successful pregnancy, but the role of MDSCs in abnormal pregnancy caused by Toxoplasma gondii infection is unknown. Herein, we revealed a distinct mechanism by which T-cell immunoglobulin domain- and mucin domain-containing protein-3 (Tim-3), an immune checkpoint receptor that balances maternal-fetal tolerance during pregnancy, contributes to the immunosuppressive function of MDSCs during T. gondii infection. The expression of Tim-3 in decidual MDSCs was significantly downregulated following T. gondii infection. The proportion of monocytic MDSC population, the inhibitory effect of MDSCs on T-cell proliferation, the levels of STAT3 phosphorylation, and the expression of functional molecules (Arg-1 and IL-10) in MDSCs were all decreased in T. gondii-infected pregnant Tim-3 gene knockout (Tim-3KO) mice compared with infected pregnant WT mice. After treatment with Tim-3-neutralizing Ab in vitro, the expression levels of Arg-1, IL-10, C/EBPβ, and p-STAT3 were decreased, the interaction between Fyn and Tim-3 or between Fyn and STAT3 was weakened, and the binding ability of C/EBPβ to the promoters of ARG1 and IL10 was decreased in human decidual MDSCs with T. gondii infection, while opposite results were observed following treatment with galectin-9 (a ligand for Tim-3). Inhibitors of Fyn and STAT3 also downregulated the expression of Arg-1 and IL-10 in decidual MDSCs and exacerbated adverse pregnancy outcomes caused by T. gondii infection in mice. Therefore, our studies discovered that the decrease of Tim-3 after T. gondii infection could downregulate the functional molecules of Arg-1 and IL-10 expression in decidual MDSCs through the Fyn-STAT3-C/EBPβ signaling pathway and weaken their immunosuppressive function, which eventually contributes to the development of adverse pregnancy outcomes.

opennotspecifiedJun 2022View details →

Fig. 7. Linear correlation between experimental and calculated 13C in Discovery of Undescribed Monoterpenoid Polyprenylated Acylphloroglucinols with Immunosuppressive Activities from Hypericum longistylum

Fig. 7. Linear correlation between experimental and calculated 13C NMR chemical shifts of 5 at the B972/pcSseg-2 (A) and mPW1PW91/def2-TZVP (B) levels.

opennotspecifiedJun 2022View details →

Fig. 8 in Discovery of Undescribed Monoterpenoid Polyprenylated Acylphloroglucinols with Immunosuppressive Activities from Hypericum longistylum

Fig. 8. Calculated and experimental ECD spectra of 5 (A) and experimental ECD curves of compounds 5, 6 and 7 (B) (in MeOH).