What are the mechanisms of rheumatoid arthritis disease?5 answersThe mechanisms of rheumatoid arthritis (RA) involve the formation of synovial villi, inflammation, immune abnormalities, and bone-cartilage destruction. In individuals with a genetic predisposition to RA, there is a tight interaction between cells and mediators of the innate and adaptive immune system, leading to the amplification and perpetuation of inflammation and tissue remodeling. The pathogenesis of RA starts years before the onset of clinical symptoms, with immune disturbance mechanisms occurring outside the joint compartment, followed by systemic immune response maturation and eventual targeting of the synovial and bone compartment. The etiology of RA is not clear, but it is characterized by chronic synovitis and symmetrical joint destruction. Treatment of RA aims to achieve remission or low disease activity, but functional disorders of the nociceptive system, such as peripheral and central sensitization, can negatively affect treatment outcomes.
What are the mechanisms underlying B cell activation?4 answersB cell activation is a complex process involving multiple mechanisms. The B cell receptor (BCR) signals together with a co-receptor complex to initiate activation in response to antigen binding. The recruitment kinetics of essential signaling effectors to the co-receptor complex, such as CD19, play a crucial role in B cell activation. Actin cytoskeleton reorganization also regulates BCR signaling during B cell activation, and impaired actin cytoskeleton can disrupt normal B cell activation. Additionally, the transduction mechanisms involved in B cell activation include receptor expression, receptor coupling to second-messenger generating systems, and cellular programming for specific responses. The BCR pathway is a potential therapeutic target in B cell malignancies, and various mechanisms have been identified for BCR pathway activation in different diseases. Understanding these mechanisms is important for developing targeted therapies for B cell-associated diseases.
Why the mechanism of Drug-Immune Cell Interactions occur?5 answersDrug-immune cell interactions occur due to the recognition of drug molecules as "non-self" by the immune system, leading to immune responses. These interactions can be mediated by various mechanisms, including hapten-carrier complex formation, direct binding of drugs to T-cell receptors (TCR) or major histocompatibility complex (MHC) molecules, and drug-protein interactions. The hapten mechanism involves drugs binding covalently to endogenous proteins, forming antigenic complexes that induce T-cell responses. The p-i concept suggests that drugs can directly interact with TCR or MHC molecules, leading to T-cell activation. Reactive drug metabolites and drug-protein interactions can also initiate immunologic events mediating adverse drug reactions. In some cases, drug-induced antibodies can bind to specific target cells, such as platelets or granulocytes, resulting in their destruction. Understanding the mechanisms of drug-immune cell interactions is crucial for identifying potential adverse reactions and developing targeted therapeutic strategies.
How the mechanism of Drug-Immune Cell Interactions occur?5 answersDrug-immune cell interactions can occur through different mechanisms. The hapten concept suggests that small chemical compounds need to bind covalently to proteins to be recognized by the immune system. However, recent evidence suggests that some drugs can directly and reversibly interact with immune receptors like the major histocompatibility complex (MHC) or the T cell receptor (TCR), stimulating the cells similar to a pharmacological activation. These interactions can lead to the activation of drug-specific T cells, resulting in hypersensitivity reactions. The mechanisms of drug interactions involve drug metabolizing enzymes, drug transporters, and orphan nuclear receptors that regulate the expression of enzymes and transporters. Inhibition of drug metabolism or transport can increase drug plasma concentrations, while induction of orphan nuclear receptors can decrease drug concentrations. The p-i concept suggests that drugs can bind directly to the TCR or the MHC molecule, leading to T cell activation. Overall, drug-immune cell interactions involve complex processes that can have diverse clinical manifestations.
List of Drug-Immune Cell Interactions?4 answersDrug-Immune Cell Interactions can be predicted using an integrative computational approach that matches gene sets between transcriptional signatures to determine their similarity. This approach has been used to model the interactions between drugs and immune cell types, resulting in the prediction of thousands of interactions. Additionally, certain immune cells and their effector molecules have been found to play a role in the regulation of drug-induced liver damage. Adverse drug events associated with cytokines and monoclonal antibodies have also been studied, with new monoclonal antibodies such as catumaxomab, daratumumab, and nivolumab being included in the analysis. The interaction between drugs and the immune system during cancer treatment has been reviewed, with a focus on drug hypersensitivity and the selective activity of drugs on lymphocytes.
What are the Drug-Immune Cell Interactions ?5 answersDrug-immune cell interactions involve the interaction between drugs and the immune system during various medical conditions such as cancer treatment and HIV infection. In cancer treatment, drugs can selectively act on lymphocytes and induce new cell antigens, affecting the immune response. In HIV-infected patients, drug interactions can be complex and practitioners need exposure-response data to predict their clinical impact. Additionally, drug-induced liver damage can activate the immune system, leading to sterile inflammation and hepatocyte death. These interactions are of special interest due to the liver's role in detoxification and its constant exposure to xenobiotics. Overall, drug-immune cell interactions play a crucial role in understanding the efficacy and safety of drug treatments in various medical conditions.