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These flashcards cover key terms and concepts related to the complement system and innate immunity, structured for effective study and review.
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Complement System
A cascade of ~30 proteins in blood plasma that kill pathogens, opsonize them, recruit immune cells, and clear immune complexes.
C3 Convertase
An enzyme complex that cleaves C3 into C3a and C3b, central to the complement system.
Classical Pathway
A complement activation pathway triggered by antibodies bound to pathogen surfaces, leading to C3 convertase formation.
Lectin Pathway
A complement activation pathway triggered by Mannose-Binding Lectin (MBL) recognizing mannose on pathogens, not requiring antibodies.
Alternative Pathway
A complement activation pathway that is always active at low levels and does not require antibodies or lectins.
Opsonization
The process by which C3b coats a pathogen's surface to enhance its phagocytosis by immune cells.
Membrane Attack Complex (MAC)
A structure formed by complement proteins that creates pores in pathogen membranes, leading to cell lysis.
C3a
A small fragment released upon C3 cleavage, acts as an anaphylatoxin and causes inflammation.
C3b
A large fragment of C3 that functions as an opsonin and is involved in forming C5 convertase.
Factor H
A regulatory protein that helps cleave C3b to inactivate it and prevent damage to human cells.
Properdin
A protein that stabilizes C3bBb, enhancing the alternative pathway's activity.
Anaphylatoxins
Small complement fragments (C3a, C4a, C5a) that trigger inflammation and recruit immune cells.
C1 Inhibitor (C1-INH)
A protein that inactivates C1r and C1s to regulate the classical pathway of complement.
C5a
The most potent anaphylatoxin, involved in chemotaxis and activation of immune cells.
C6
A component of the complement system that binds C5b during the formation of the MAC.
C7
A component of the MAC that participates in the formation of the transmembrane pore.
C9
A complement protein that polymerizes to form the large pore in the membrane during MAC formation.
Phagocytosis
The process by which phagocytes engulf and destroy pathogens or particles.
Fluid-phase convertase
A weak C3 convertase formed in blood during the alternative pathway's tickover.
Decay Accelerating Factor (DAF)
A protein on human cells that prevents the formation of the C3 convertase.
Membrane Cofactor Protein (MCP)
A human cell surface regulator that helps inactivate C3b by aiding Factor I.
C-reactive protein (CRP)
An acute phase protein produced in response to inflammation, functioning as an opsonin.
C4 Binding Protein (C4BP)
A protein that accelerates the decay of the complement C3 convertase.
Iron sequestration
A process by which the body hides iron from pathogens to inhibit their growth.
Bradykinin
A mediator of pain, inflammation, and increased vascular permeability; derived from the kinin system.
IL-1
A cytokine produced by macrophages that induces fever and activates T cells.
IL-6
A cytokine produced in response to inflammation that promotes immune responses and fever.
TNF-α
A pro-inflammatory cytokine that has multiple effects including fever and activation of the endothelium.
IL-10
An anti-inflammatory cytokine that inhibits TH1 cells and macrophage activation.
Anemia of Chronic Disease
A condition characterized by low serum iron despite normal stores, due to sequestration in macrophages.
Septic Shock
A severe systemic inflammatory response often mediated by anaphylatoxins like C5a.
Chemotaxis
The movement of immune cells toward the site of infection or inflammation in response to chemical signals.
Hapto globin
A complement protein that binds free hemoglobin, preventing oxidative damage.
Eculizumab
A monoclonal antibody used to inhibit MAC formation by blocking C5.
Hereditary Angioedema
A condition caused by deficiency of C1-INH leading to uncontrolled classical pathway activation.
Dark urine
A clinical sign of hemolysis, often seen in conditions like Paroxysmal Nocturnal Hemoglobinuria.
Positive feedback loop
A mechanism where an increase in a process leads to further increases, such as C3b generating more C3 convertase.
Nth disease
A term referring to recurrent infections due to complement deficiencies.
Cytokine-blocking Drugs
Therapeutics such as monoclonal antibodies that target and inhibit specific cytokines involved in inflammation.