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The Scientific Basis of Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Chris O'Callaghan, Rachel Allen
Key cells of the innate immune system include phagocytes, such as macrophages and dendritic cells, which destroy exogenous particles by phagocytosis and can process ingested proteins for presentation to T cells. Through this process, dendritic cells are able to prime naive T cells. Recognition of microbial components or damage-associated molecular patterns by innate immune receptors on phagocytes can elicit the production of cytokines, which in turn trigger inflammation and inform the responses of other immune cells.
Drug Allergy
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
Another mechanism is known as the pharmacologic interaction with immune receptors or ‘p-i concept’. Here, drugs bind noncovalently with T-cell receptors leading directly to a T cell response without requiring previous sensitization. This mechanism may account for some drug reactions that occur on first exposure to the agent.
Monoterpenes Modulating IL-10
Published in Parimelazhagan Thangaraj, Phytomedicine, 2020
Saravanan Shanmugam, Jullyana S. S. Quintans, Parimelazhagan Thangaraj, Luciana Scotti, Marcus T. Scotti, Adriano A. S. Araújo, Lucindo J. Quintans-Júnior
Oxidative stress plays a significant role in the pathogenesis of inflammatory disorders, inflammation is the immune system’s response to fight against the external pathogens or internal injury. The inflammatory response is triggered by innate immune receptors that recognize pathogens and damaged cells. The overexpression of the pro-inflammatory mediators, such as reactive oxygen mediator, neutrophil infiltration, and cytokines has been known to contribute to the inflammatory cascade in the pathological process of colitis (Neurath 2014). Moreover, the nuclear transcription factor kappa B (NF-κB) is identified as one of the pivotal regulatory components in inflammatory diseases and inhibition of its activity may alleviate the severity of the inflammation process (Liu et al. 2017).
A PD-L1/EGFR bispecific antibody combines immune checkpoint blockade and direct anti-cancer action for an enhanced anti-tumor response
Published in OncoImmunology, 2023
Laura Rubio-Pérez, Rodrigo Lázaro-Gorines, Seandean L. Harwood, Marta Compte, Rocío Navarro, Antonio Tapia-Galisteo, Jaume Bonet, Belén Blanco, Simon Lykkemark, Ángel Ramírez-Fernández, Mariola Ferreras-Gutiérrez, Carmen Domínguez-Alonso, Laura Díez-Alonso, Alejandro Segura-Tudela, Oana Hangiu, Ainhoa Erce-Llamazares, Francisco J. Blanco, Cruz Santos, José L. Rodríguez-Peralto, Laura Sanz, Luis Álvarez-Vallina
Modulating immune responses using monoclonal antibodies (mAbs) is one of the most promising approaches for cancer immunotherapy1]. Immune checkpoints are coinhibitory and costimulatory receptors that are crucial for maintaining self-tolerance and modulating immune responses2. However, inhibitory checkpoints can be “hijacked” by tumors to evade immune responses3. MAb-based blockade of coinhibitory immune receptors, such as cytotoxic T lymphocyte antigen 4 (CTLA-4), programmed cell death-1 (PD-1) receptor, or PD-1 ligand (PD-L1) has shown durable tumor clinical responses in a wide range of cancer types, but their efficacy is limited to 10% to 30% of patients4. Different factors, such as the tumor mutational burden and immunogenicity of cancer cells, the composition of the tumor microenvironment (TME) and the degree of immune cell infiltration, influence the response to immune checkpoint blockade (ICB)5. Increasing the response rates to ICB is likely to require the design of therapeutic combinations that are tailored to the aforementioned factors6. On the other hand, EGFR is a receptor tyrosine kinase well-known as a tumor-associated antigen (TAA) with an important functional role, since EGFR deregulation promotes proliferation, apoptosis inhibition and invasion of cancer cells7. Therefore, mAb targeting EGFR not only mark tumor cells for immune killing but also may inhibit phosphorylation of key intracellular tyrosine residues, thus preventing ligand-mediated mitogenic signaling8.
Recent trends in the development of Toll-like receptor 7/8-targeting therapeutics
Published in Expert Opinion on Drug Discovery, 2021
Xuan Huang, Xiaoyong Zhang, Mengji Lu
Toll-like receptors (TLRs) are a group of the well-studied pattern recognition receptors [4]. They are highly conserved innate immune receptors present in multiple host cells and tissues. Since TLR4 and its ligand LPS were first discovered in 1997 and 1998, respectively, [5,6], other members of the TLR family and their corresponding ligands have been identified [7,8]. To date, 10 functional TLRs have been discovered in humans (TLRs 1–10), and a further three have been discovered that are expressed only in mice (TLRs 11–13) [9–11]. In humans, TLRs 1, 2, 4, 5, and 6 are mainly expressed on the cell surface, where they respond primarily to bacterial macromolecules including lipoproteins and LPS [12–15]. TLRs 3, 7, 8, 9, and 10 are located intracellularly, and they are activated mainly by foreign nucleic acids passed into cells during infection [16–20]. TLRs have an extracellular domain, a transmembrane domain, and a cytosolic toll-interleukin (IL)-1 receptor domain [21,22]. The extracellular domain is a leucine-rich repeat (LRR) region that can recognize and bind to pathogen-associated molecular patterns and DAMPs. The transmembrane domain and the cytosolic toll-IL-1 receptor domain coordinate downstream signaling pathways [23,24].
Green synthesis of silver nanoparticles from Eriobotrya japonica extract: a promising approach against cancer cells proliferation, inflammation, allergic disorders and phagocytosis induction
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2021
Majid S. Jabir, Aya A. Hussien, Ghassan M. Sulaiman, Nahi Y. Yaseen, Yaser H. Dewir, Mona S. Alwahibi, Dina A. Soliman, Humaira Rizwana
When a person has cancer, inflammation, which is a non-specific immune response to infection, irritation or other injuries, begins with redness, fever, swelling, pain, and loss of function. The inflammation is triggered by innate immune receptors that recognize pathogens and damaged cells. The purpose of inflammation is to eliminate the initial cause of cell injury and remove necrotic cells and tissues damaged from the original injury and the inflammatory process to initiate tissue repair. Therefore, the inflammatory response is essential to remaining healthy and maintaining homeostasis. However, the inflammatory process does not always result in the successful resolution and repair of damaged tissue. Allergic disorders are a growing international pathological state for over 25% of populations in industrialized countries, and a significant worldwide increase has occurred in the prevalence of respiratory disease and rhinitis since 1960 [11].