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β-catenin Signalling in Immune-Metabolism Landscape
Our research investigates β-catenin’s role in Toxoplasma gondii infection and how its inhibition mitigates infection by promoting an anti-inflammatory environment. We will examine the metabolic changes, focusing on enhancing oxidative phosphorylation and the pentose phosphate pathway, and their effects on immune tolerance. Additionally, we will explore gut microbiota alterations and the role of compromised mitophagy and mitochondrial trafficking in supporting parasite growth. By promoting mitochondrial fitness, we aim to suppress inflammation, marked by increased IL-10 and TGF-β, and a transition of T-cells to Th2, Treg, and ThPD1 subsets, developing comprehensive therapeutic strategies
Placental Metabolic Imbalance Disrupts Neuro-Immune Homeostasis in Offspring
Our research explores how Toxoplasma gondii infection disrupts mTOR-NLRP3 signaling, causing cognitive disorders through CNS inflammation. We examine the parasite's ability to breach the placenta, affecting fetal brain development and immune maturation. We focus on how altered microbiota and metabolites impact placental trophoblasts and brain-centric T-cells. We investigate mitochondrial dysfunction, mitophagy, and ROS generation in placental and brain cells. Using infected pregnant mice and cell models, we aim to correlate these changes with neuroinflammation and cognitive impairments in offspring. Our goal is to identify therapeutic strategies targeting mTOR-IRF signaling to enhance mitochondrial fitness and mitigate cognitive disorders.
Immune Modulation in Circadian Rhythm
Our research focuses on understanding the link between Toxoplasma gondii infection and circadian disorders through the microbiome and BMAL1-CLOCK signaling. We will investigate BMAL1-CLOCK activation and its role in homeostasis and inflammation. We aim to dissect microbiota's role in tryptophan catabolism and its impact on circadian rhythms, exploring how microbiota shapes T-cell differentiation and inflammation. Using humanized mice and single-cell sequencing, we will study microbiota-tryptophan imbalances and T-cell responses. Our goal is to develop intervention strategies, including nutritional approaches and genetically modified bacteria, to restore circadian behavior and reduce brain inflammation, potentially leading to identifying therapeutic solutions.
Immunoinformatics and Reverse Vaccine Technology
Our strategy employs reverse vaccinology to combat Helicobacter pylori infections. We aim to identify T-cell epitopes that bind multiple HLAs, select TLR ligands to enhance antigenicity, and validate a chimeric nano/micro-particle for oral delivery to elicit gut-localized immune responses. This approach mimics pathogen components using PAMPs and protein antigens, facilitating IL-12-driven Th1 differentiation essential for protective immunity. Advantages include expelling H. pylori, generating memory responses, and avoiding drug resistance.
Our research develops a multi-epitope vaccine targeting Monkeypox virus by mapping highly immunogenic epitopes from structural glycoproteins. The vaccine formulation includes adjuvants and linkers for enhanced stability and immunogenicity. Molecular dynamics simulations predict strong interactions with immune receptors, supporting robust memory immune responses and protective immunity in silico.
Targeting DPP4 to Mitigate SARS-CoV-2 Infection: Gliptins' Efficacy Revealed
Our research demonstrated that the SARS-CoV-2 spike protein's receptor binding domain (RBD) interacts with human DPP4, aiding virus entry alongside ACE2. We identified that RBD forms hydrogen bonds and hydrophobic interactions with DPP4’s α/β-hydrolase domain. Using inhibitors like sitagliptin and linagliptin, we prevented RBD from binding both DPP4 and ACE2, thereby inhibiting viral entry and replication. These inhibitors effectively mitigate the growth of various SARS-CoV-2 variants, including alpha, beta, delta, and kappa, proposing a novel strategy to combat COVID-19.
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