Does IL-1 beta induce the expression of adhesion molecules on T cells?5 answersIL-1 beta has been shown to induce the expression of adhesion molecules on T cells. Studies have demonstrated that IL-1 beta treatment of human umbilical vein endothelial cells (HUVEC) leads to the induction of new membrane proteins, including a major inducible sialoglycoprotein that is distinct from ELAM-1 and plays a role in T cell-endothelial cell adhesion events. Additionally, cytokines like macrophage inflammatory protein-1 beta (MIP-1 beta) have been identified as inducers of T cell adhesion to endothelium, particularly through the augmentation of binding to VCAM-1. Furthermore, the upregulation of ICAM-1, an adhesion accessory molecule, on human beta-cells by cytokines like IL-1 beta facilitates T-lymphocyte recognition of beta-cell autoantigens. Therefore, IL-1 beta does induce the expression of adhesion molecules on T cells through various mechanisms.
What are the potential therapeutic targets for modulating IL-17 signaling in the treatment of lung cancer?4 answersPotential therapeutic targets for modulating IL-17 signaling in lung cancer treatment include targeting the IL-17A/IL-17RC axis, inhibiting the p38 MAPK signaling pathway, focusing on IL-17-mediated regulation of the tumor immune microenvironment, and considering IL-17 as a viable therapeutic approach for COPD management, which shares pathophysiological similarities with lung cancer. Additionally, targeting IL-17A to prevent tobacco smoke-induced EMT in lung cancer by regulating the expression of ΔNp63α and miR-19 could be a promising strategy. Understanding the role of ADAM17 in the development of lung adenocarcinoma and its potential as a therapeutic target to inhibit IL-6 trans-signaling and EGFR family ligands also presents a promising avenue for treatment.
What are the potential therapeutic targets for modulating the relationship between IL17 and TNF in autoimmune disorders?5 answersTargeting the relationship between IL-17 and TNF in autoimmune disorders presents promising therapeutic avenues. IL-17, produced by Th17 cells, plays a crucial role in autoimmune diseases like psoriasis and lupus. On the other hand, TNFα is an inflammatory cytokine implicated in autoimmune diseases. Modulating the balance between regulatory T-cells (Tregs) and pro-inflammatory Th17 cells is crucial in autoimmune disorders. Studies have highlighted the therapeutic potential of targeting IL-17 in immune disorders, given its role in promoting autoimmune tissue inflammation. Therefore, strategies that aim to neutralize IL-17 or TNFα, or modulate the Th17/Treg balance, could offer effective treatment options for autoimmune diseases by addressing the interplay between these cytokines.
Down syndrome - Neurobiological alterations and therapeutic targets4 answersDown syndrome is a genetic disease caused by an aneuploidy of human chromosome 21, leading to cognitive and learning deficits. Neurobiological alterations in Down syndrome include impairments in GABAergic and glutamatergic transmission, mitochondrial dysfunction, increased oxidative stress and inflammation, and DNA hyper-methylation. Mouse models of Down syndrome have provided insights into the molecular and cellular changes associated with the disease, particularly in the brain. Pharmacological therapies targeting these alterations have shown promise in improving cognitive function in mouse models, with a focus on synaptic plasticity, neurogenesis, and neuromodulatory systems. Several potential therapeutic targets have been identified, including the choline pathway, GABA and NMDA receptors, DYRK1A protein, oxidative stress pathways, and neurogenesis-related pathways. Clinical trials have been conducted with some of these targets, but more research is needed, especially in the prenatal period, to improve cognitive outcomes in individuals with Down syndrome.
What is the role of IL1 beta1 in the pathogenesis of epilepsy and cognitive comorbidity ?4 answersThe role of IL-1β in the pathogenesis of epilepsy and cognitive comorbidity is still being investigated. There is evidence that IL-1β signaling in the hippocampus may be a mechanistic factor in both temporal lobe epilepsy (TLE) and clinical depression. Studies have shown increased IL-1β expression in brain tissue from epilepsy patients and animal models after seizures. Additionally, IL-1β has proconvulsive properties when applied exogenously. However, there are opposing results in the literature, and more research is needed to fully establish the role of IL-1β in seizure generation and epilepsy. The pathophysiological mechanisms of cognitive impairment in epilepsy are complex and involve alterations in signaling pathways and neuronal network function. Prolonged or recurrent seizures can cause or exacerbate cognitive impairment, although the biological underpinnings of cognitive impairment may be distinct from the processes that cause seizures.
Does interleukin-1 beta disrupt thyroid function?4 answersInterleukin-1 beta (IL-1 beta) has been shown to have both inhibitory and stimulatory effects on thyroid function. It has been found to decrease iodide uptake and organification, as well as inhibit the secretion of thyroglobulin and cyclic AMP (cAMP). However, at low concentrations, IL-1 beta has been shown to enhance the secretion of thyroglobulin and cAMP. IL-1 beta has also been found to stimulate the secretion of T3, but not T4, and this effect is dose-dependent. These findings suggest that IL-1 beta may play a role in the pathogenesis of autoimmune thyroid diseases and may regulate thyroid function under physiological conditions. IL-1 beta does not appear to directly influence the growth of thyroid follicles. Overall, IL-1 beta can disrupt thyroid function by affecting iodide metabolism, thyroglobulin secretion, and cAMP production, but its exact role in thyroid diseases requires further investigation.