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Flashcards covering the molecular and cellular basis of autoimmune diseases, the 5 Rs of inflammation, mediators of acute and chronic inflammation, and tissue repair processes.
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Autoimmune Malfunction
A condition where the immune system recognizes auto-antigens in its own molecules, cells, or structures due to a lack of tolerance.
Macrophage specific folate receptor (FRb)
An innate immune system mediator in tissue-resident macrophages that acts as a sensor for adjusting effector functions to extracellular folate levels and can polarize between proinflammatory and anti-inflammatory states.
M-Mø
Anti-inflammatory, M−CSF-dependent IL−10 human macrophages.
Th17 subset
A cell population involved in host defense and cell-mediated inflammation, linked to pathologies such as RA, Crohn’s disease, and Systemic Lupus Erythematosus (SLE).
Thymic epithelial cells (TECs)
Cells involved in the environment of the thymus that interact with thymocytes (T) and ephrins (Eph) to modulate the adaptive immune response through intra-thymic selection.
Vasoactive Intestinal Peptide (VIP)
An anti-inflammatory and immunomodulatory neuropeptide released by nerve endings and immune cells that modulates senescent Th biomarkers.
Adipokines
Adipose tissue derived factors, such as adiponectin, leptin, visfatin, and restin, that act as inflammatory cytokines and metabolic factors.
5 Rs of Inflammation
The clinical steps of the inflammatory response: Recognition of the agent, Recruitment of leukocytes, Removal of the agent, Regulation of the response, and Resolution (repair).
Steps of Acute Inflammation
A process involving vasodilation (after transient vasoconstriction), increased vascular permeability, and chemotaxis.
Transudate
An extravascular fluid with low protein content (mostly albumin), low specific gravity, and very few cells.
Exudate
An extravascular fluid with high protein content, high specific gravity, and a high amount of cells and debris.
Edema
The accumulation of excess fluid in interstitial tissue.
Vasodilation Mediators
Chemical substances including Histamine, Prostaglandin (PGI2), and Nitric Oxide responsible for increasing blood vessel diameter during acute inflammation.
Pavementing
The stage of leukocyte recruitment facilitated by LFA−1 and Mac−1 on white blood cells and ICAM−1 and VCAM−1 on the endothelium.
CD31 (PECAM)
A mediator found on both white blood cells and the endothelium that facilitates the transmigration of leukocytes.
Opsonins
Substances such as IgG, C3b, and Collectins that coat particles to promote their removal by the immune system.
Healing (Fibrosis)
A repair outcome resulting in the formation of a scar, typically occurring when the tissue cannot completely replace damaged cells.
Regeneration
The complete replacement of damaged cells with original tissue types resulting in no scar formation, requiring an intact connective tissue scaffold.
Granulation Tissue
Specialized tissue formed 3-5 days into the scarring process, characterized by the formation of new blood vessels and fibroblast proliferation.
Vascular Endothelial Growth Factor (VEGF)
A mediator in the repair process that induces the formation of new blood vessels (angiogenesis).
Transforming Growth Factor-beta (TGF-b)
A mediator that acts as a growth inhibitor for epithelium and is produced by activated macrophages to promote scarring.
Platelet Derived Growth Factor (PDGF)
A mediator that promotes the migration and proliferation of fibroblasts, smooth muscle cells, and monocytes during tissue repair.
Healing by First Intention
The repair of a wound with clean edges and minimal tissue disruption, such as a surgical incision, resulting in a small to nonexistent scar.
Healing by Second Intention
The repair of a wound with unclean edges, extensive tissue disruption, and necrosis, such as a cutaneous ulcer, resulting in a prominent scar.