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Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
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Inflammation01:38

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Overview
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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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T Cell Types and Functions01:24

T Cell Types and Functions

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

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Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
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Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
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[DAMPs (damage-associated molecular patterns) and inflammation].

Hiroaki Ooboshi, Takashi Shichita

    Nihon Rinsho. Japanese Journal of Clinical Medicine
    |June 24, 2016
    PubMed
    Summary
    This summary is machine-generated.

    Post-ischemic inflammation drives ischemic stroke progression. Damage-associated molecular patterns, like peroxiredoxin, activate immune cells, leading to delayed infarct expansion and suggesting new therapeutic targets.

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    Area of Science:

    • Neuroscience
    • Immunology
    • Pathology

    Context:

    • Ischemic stroke progression is significantly influenced by post-ischemic inflammation.
    • Damage-associated molecular patterns (DAMPs) activate inflammatory cells through Toll-like receptors (TLR2 and TLR4).
    • Key DAMPs include high mobility group box-1 (HMGB-1) and heat shock proteins.

    Purpose:

    • To investigate the role of peroxiredoxin (Prx) as a DAMP in brain ischemia.
    • To elucidate the inflammatory cascade involving macrophages, IL-23, and γδT cells.
    • To identify novel therapeutic targets for ischemic stroke treatment.

    Summary:

    • Peroxiredoxin (Prx) acts as a potent DAMP, activating infiltrating macrophages in the context of brain ischemia.
    • Activated macrophages release interleukin-23 (IL-23), which stimulates γδT cells.
    • These γδT cells subsequently release IL-17, contributing to delayed expansion of infarct lesions.

    Impact:

    • Highlights the critical role of the innate immune response in ischemic stroke pathogenesis.
    • Suggests that targeting the Prx-macrophage-IL-23-γδT cell axis could offer novel therapeutic strategies.
    • Presents potential for developing stroke treatments with a broader therapeutic time window.