scispace - formally typeset
Search or ask a question

What are the mechanisms of endocrine-immune interactions? 

Best insight from top research papers

The mechanisms of endocrine-immune interactions involve a bidirectional communication between the two systems. The immune system and the neuroendocrine system share common features and use similar molecules and receptors for communication . Hormones, cytokines, neuropeptides, and neurotransmitters play a role in modulating the host immune response . Parasites can influence the host's endocrine status and alter hormone levels . Lipopolysaccharide (LPS) from gram-negative bacteria can directly modify the physiology of the anterior pituitary and affect hormone production . The immune system-derived thyroid stimulating hormone (TSH) controls thyroid hormone synthesis and bone metamorphosis . The cross-regulation of endocrine and immune mechanisms in pro- and anti-inflammatory responses is not fully understood . Understanding these mechanisms is important for developing new therapies for infectious diseases .

Answers from top 4 papers

More filters
Papers (4)Insight
The paper discusses the mechanisms of endocrine-immune interactions, specifically focusing on the effects of lipopolysaccharide (LPS) on pituitary physiology and the molecular mechanisms involved.
The paper discusses the dynamic interactions between the immune system and the neuroendocrine system, but it does not specifically mention the mechanisms of endocrine-immune interactions.
The paper discusses the close relationship between hormones, cytokines, neuropeptides, and neurotransmitters that modulate the host immune response. It mentions that disruption of this communication balance can result in disease or higher susceptibility to infections. However, it does not provide specific mechanisms of endocrine-immune interactions.
The paper discusses the principal mechanisms of bi-directional communication between the neuroendocrine and immune systems.

Related Questions

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.

See what other people are reading

Why is there a need for alternative strategies to combat microbial infections?
5 answers
The need for alternative strategies to combat microbial infections arises due to the emergence of antibiotic-resistant bacteria and the prevalence of illnesses linked to biofilms. Traditional antibiotics are becoming increasingly limited in their effectiveness, as more bacteria develop resistance to them. Therefore, there is an urgent need to develop new approaches to control bacterial infections. Promising strategies include the development of therapeutic vaccines, the utilization of innate immune activation techniques, and the use of metal-carrying formulations. Nanoparticle-based materials have also gained interest for their antimicrobial properties. Additionally, alternative treatment strategies focus on targeting toxin secretion systems, biofilm formation, and adhesion mechanisms that affect quorum sensing of microbial populations. Other non-antibiotic mechanisms of action, such as phage therapy, microbiota-modulating therapies, and enhancing immune response, are also being explored. Overall, alternative strategies are needed to address the limitations of traditional antibiotics and combat the growing problem of antibiotic resistance.
What are the key factors that contribute to wound healing?
5 answers
Wound healing is a complex process that involves multiple factors. Local factors such as oxygenation and infection, as well as systemic factors including age, gender, stress, diabetes mellitus, obesity, drugs, alcohol, smoking, and nutrition, can all affect wound healing. Electric factors, such as electric charges, electrodynamic field, and interstitial exclusion, also play a role in wound healing physiology and can be targeted for treatment. The human wound-healing process consists of four phases: hemostasis, inflammatory, proliferation, and remodeling, and various factors can hinder these phases, including interferon, stem cells, chronic venous ulcer, chronic fistula, bionanomaterials, topical antiseptic agents, diabetic ulcers, and nutritional supplements. Blood and lymphatic vessels are crucial for tissue regeneration and healing, with angiogenesis and lymphangiogenesis being important processes. Angiogenic factors like VEGF-A and macrophages play a role in angiogenesis, while VEGF-C or -D and lymphatic vessel endothelial hyaluronan receptor-1-positive macrophages are involved in lymphangiogenesis. Additionally, factors such as local necrosis and infection, increased pressure and edema, anemia, hypoxia, hypotension, chronic diseases, medication, immunosuppression, nutritional status, age, and body constitution can influence burn wound healing.
What is the mechanism of immune gene response against viral infection?
4 answers
The mechanism of immune gene response against viral infection involves the recognition of virus-derived components by immune surveillance sensors, leading to the production of type I interferons, pro-inflammatory cytokines, and chemokines by host cells. These immune surveillance sensors, such as TLR, RIG-I, and cGAS-STING axis, detect virus-derived nucleic acids in the cytosol or intracellular compartments. The primary sensing of virus-derived nucleic acids by these sensors triggers the activation of adaptor molecules and intracellular kinases, ultimately leading to the initiation of antiviral responses. However, viruses have also evolved counteracting strategies to evade the immune response by targeting immune sensors, adaptor molecules, kinases, and transcription factors. The host defense machinery against viral infection is tightly regulated to prevent aberrant immune responses to self and non-self-nucleic acids.
Does the prefrontal cortex play a role in depressive-like behaviors?
5 answers
The prefrontal cortex (PFC) does play a role in depressive-like behaviors. Depletion of astroglia expressing glial fibrillary acidic protein (GFAP) in the PFC induces anhedonia-like behavior in rodents. Activation of PFC GFAP+ cell activity reverses anhedonia-like deficits induced by chronic stress. In addition, acute stressful stimuli can cause supersensitivity of P2X7Rs in the PFC, facilitating the learned helplessness reaction associated with depression. Furthermore, protein phosphatase Mg2+/Mn2+-dependent 1F (PPM1F) in the medial PFC modulates depression-related behavioral responses. Ultrasound stimulation of the PFC can improve depressive-like behaviors, possibly through the downregulation of inflammatory cytokines in the PFC. These findings highlight the importance of the PFC in the development and modulation of depressive-like behaviors.
What are the main pathways of pathogenesis of asthma?
4 answers
The main pathways of pathogenesis of asthma involve various molecular processes and complex molecular pathways. These include regulatory metabolism, Fc gamma-R mediated phagocytosis, leukocyte transendothelial migration, tumor necrosis factor signaling pathway, Toll-like receptor signaling pathway, B cell receptor signaling pathway, phosphoinositol 3-kinase/protein kinase B signaling pathway, vascular smooth muscle contraction, and cell adhesion signaling pathway. Additionally, immunoglobulin E, cytokines, nitric oxide, dendritic cells, leukotrienes, oxidative stress, and inflammatory infiltrate of mast cells, neutrophils, eosinophils, lymphocytes, innate immunity, and other factors contribute to the development and progression of asthma. Furthermore, response to chemical stimulus, extracellular region, pathways in cancer, and arachidonic acid metabolism are significantly enriched terms in the bronchial epithelium of asthmatics. The lipoxygenases and their metabolites are also potential targets for the development of new drugs for asthma treatment.
What cells secrete chemokines?
4 answers
Chemokines are secreted by a wide range of immune cells, including mast cells, leukocytes, tumor cells, and natural killer (NK) cells. Mast cells, which are hematopoietic cells found in various tissues, are known to produce a broad spectrum of cytokines and chemokines in response to immune or non-immune stimuli. Leukocytes, including macrophages, neutrophils, dendritic cells, B cells, and T cells, also secrete chemokines as part of their immune response. Tumor cells have been shown to produce chemokines that control the leukocyte infiltrate and influence tumor growth and progression. NK cells, when activated by IL-2 and treated with certain drugs, upregulate the expression of chemokine receptors and secrete chemokines that induce chemotaxis and mobilization of immune cells. Overall, a variety of immune cells secrete chemokines to regulate immune responses, inflammation, and cell migration.
What is the staphylococcus Aureus?
5 answers
Staphylococcus aureus is a Gram-positive, coagulase-positive pathogen that is often present asymptomatically on parts of the human body. It is a commensal and a leading cause of bovine mastitis. S. aureus can cause a wide range of illnesses in humans, including mastitis, bacteraemia, and foodborne intoxication. It is also known for antibiotic-resistant strains such as methicillin-resistant S. aureus (MRSA), which has become an important factor in hospitals and healthcare-associated infections. MRSA is a multidrug-resistant pathogen that reduces treatment options and increases the cost of healthcare. S. aureus produces heat-resistant enterotoxins, making it a concern in temperature-abused ready-to-eat foods. However, its public health and economic impact have been minimized due to improved food safety practices. S. aureus is a frequent commensal of all humans, and precautions such as handwashing and appropriate use of gloves are necessary to reduce the risk of contamination in food preparation.
Nf-kb promotes expression of IL-8?
4 answers
NF-kB promotes the expression of IL-8.
Does NF-κB promote expression of IL-8?
4 answers
NF-κB promotes the expression of IL-8.
How do functional immune cells interact with each other?
4 answers
Functional immune cells interact with each other through intercellular communication and physical associations. These interactions play a crucial role in immune responses and maintaining tissue homeostasis. Innate lymphoid cells (ILCs) have been identified as regulators of the adaptive immune system, with reciprocal interactions between ILCs and adaptive immune cells influencing tissue immune responses. Astrocytes, a type of glial cell in the central nervous system, interact with various immune cells, including microglia, NK cells, and T cells, contributing to the pathogenesis of neurological diseases. Intercellular interactions between immune cells are mediated by ligand-receptor pairs, and nonhematopoietic stromal cells use the most network communications in the immune cell interaction network. The human immune system's intercellular wiring involves direct protein interactions between immune cells, which can modulate immune responses and maintain intercellular associations. These findings highlight the importance of functional interactions between immune cells in coordinating immune responses and potential therapeutic interventions.
What is chronic inflammation ?
5 answers
Chronic inflammation is a prolonged and unresolved state of inflammation in the body that can lead to the onset of various diseases. It is characterized by the production of free radicals and increased oxidative stress. Chronic inflammation can be caused by factors such as aging, persistent infection, and chronic non-infectious diseases like cancer, diabetes, and arthritis. It is considered the main pathophysiological cause of many disorders and can exacerbate tissue damage in different organs. Chronic inflammation is also associated with immune cell senescence and the acquisition of an inflammatory senescence-associated secretory phenotype (SASP). This low-grade chronic inflammation, known as "inflammaging," is commonly observed in aging individuals. Chronic inflammation plays a crucial role in the development of autoimmune diseases and is considered the progenitor of all human diseases. It is associated with conditions such as cardiovascular disease, cancer, diabetes, and autoimmune diseases.