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36 Cards in this Set
- Front
- Back
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The prominent cell of acute inflammation
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neutrophil
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Prominent cells of chronic inflammation
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T cells and mononuclear phagocytes
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5 signs of inflammation
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swelling, redness, pain, heat and loss of function
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1st immune cells to respond to infection
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NK cells
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viral cell infection can lead to reduced MHC 1expression. What are the implications?
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reduced CD8+ T cell recognition but NK cells target cells with reduced MHC 1 expression (also seen in tumour cells)
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what cytokines may be released from a virally infected cell
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type 1 IFN
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what do chemokines do?
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chemotactic cytokines, attract cells with appropriate receptors to site along concentration gradient. This is chemotaxis.
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prior to proteolytic activation many complement proteins exist as what?
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Proenzymens
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3 complement pathways
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classical, alternative, lectin
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classical pathway is activated by
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Antibodies
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function of the complement system
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kill target cells, enhance phagocytosis, increase leukocyte recruitment
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first step in classical pathway
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C1 (q2r2s) activated by IgM or IgG
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activated C1 does what?
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cleaves C2 and C4, C4b2b complex formed (C3 convertase), C2a and C4a released
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What composes C3 convertase and what does it do?
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C4b2b, converts C3 to C3a (released) and C3b (binds with C3 convertase to form C4b2b3b - C5 convertase)
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what initiates the alternative pathway
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in presence of bacterial surface proteins natural C3 breakdown allows C3b to bind to pathogen where it binds plasma factor B. Cleaved by plasma factor D to alternative C3 convertase (C3bBb)
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What happens in the lectin pathway prior to it joining the classical pathway
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MBL (or ficolins) bind to mannose residues on pathogen. Activates MBL-associated serine proteases MASP-1 and MASP-2 to form an activated C!-like complex.
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what happens after C5 convertase is formed
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C5a released, C5b recruits C6, C7 and C8 on microbe surface. C7 & 8 infiltrate plasma membrane, C8 recruits C9 which polymerises (10-16 residues) to form the MAC
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how does the MAC function
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prevents ion balance
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primary complement component that acts as an opsonin
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C3b
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What cells have CR1, what is it
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complement receptor 1, binds C3b opsonins, aids phagocytosis by neutrophils and macrophages
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what factors inhibit complement activation
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C1 inhibitor, Decay Accelerating Factor (breaks down C3 convertase), CD59 (inhibits C9 polymerisation)
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what do C3a and C5a released fragments do
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phagocytic chemoattractants, mast cell degranulation
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what do mast cell granules contain and what do they do
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histamine
Eicosanoids- prostaglandins (PGE2)- dilation - leukotrienes vasodilation, neutrophil chemoattractant TNF alpha- endothelial junction gaps IL1- endothelial junction gaps bradykinin- vasodilation, pain IL8 (neutrophil chemoattractant) |
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mast cell degranulation causes
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vasodilation (increased blood flow), histamine induces early endothelial contraction (vascular permeability), TNF alpha, bradykinin and IL1 (more persistant permability). Bradykinin also causes pain
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what Ig can couse mast cell degranulation
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IgE allergy
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what act as chemoattractants for inflammation
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IL8, leukotrienes (LTB4), C5a
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what cause vasodillation
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PGE2, bradykinin, histamine,
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what causes increased vascular permability
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histamine, IL1, TNF alpha
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what causes endothelial expression of extravasation receptors
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IL1, TNF alpha
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endothelial response to inflammation mediators
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more circular (gaps), cytokine release (increase inflammation), Platelet Activating Factor PAF and NO (vasodilation), express adhesion molecules (diapedesis)
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Adhesion molecules
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integrins, ICAM-1, selectins
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4 steps to extravasation
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rolling, tethering, arrest, diapedesis
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adhesion molecule interactions between neutrophil and endothelial cell
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endothelium E selectin to N CD15,
E releases IL8 turns N LFA1 active to bind to E ICAM1 |
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stages of phagocytosis
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pseudopodia, engulf, phagosome, respiratory burst, lysosome fusion, lysosomal enzymes, acidification, metabolism of material, debis release
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2 toxic compounds inside phagocyte prior to enzymes
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hydrogen peroxide, hypochlorite ions
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4 main proinflammatory cytokines
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IL1,6,8 and TNF alpha
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