Term
| What is the role of innate immunity in bacterial infections? |
|
Definition
| Innate immunity serves to phagocytose extracellular pathogens with the use of acute phase proteins produced in the liver. Acute phase proteins are produced in response to IL-6 which is secreted by macrophages |
|
|
Term
| What is the role of innate immunity in viral infections? |
|
Definition
| innate immunity functions to lyse virally infected cells via natural killer cells and activating cytotoxic T cells. Macrophages secrete IL-12 and INF I, which activates natural killer cells and T helper cells (1) which activate cytotoxic T cells |
|
|
Term
| Macrophages role in mediating mechanisms of innate immunity |
|
Definition
|
|
Term
| Neutrophils role in mediating mechanisms of innate immunity |
|
Definition
| engulf, degrate and destroy via pathogens via intracellular granules |
|
|
Term
| Natural Killer cells role in mediating mechanisms of innate immunity |
|
Definition
| lyse virally infected cell and produce cytokines |
|
|
Term
|
Definition
| Stimulates synthesis of acute-phase and complement proteins in the liver |
|
|
Term
|
Definition
| Systemic (fever) and Local (tumor, rubor, calor, dolor) inflammation |
|
|
Term
|
Definition
| Lymphocytes’ activation, Production of IL-6 |
|
|
Term
|
Definition
| Chemotaxis: accumulation of inflammatory cells in the center of reaction |
|
|
Term
|
Definition
| NK and T helper cell 1 activation |
|
|
Term
|
Definition
| Chemotaxis is the accumulation of inflammatory cells in the center of the reaction |
|
|
Term
|
Definition
|
|
Term
|
Definition
| regulated by CAMs and chemokines |
|
|
Term
|
Definition
| white blood cells to the site of infection |
|
|
Term
| Phagocytic receptor function of the macrophage |
|
Definition
| Phagocytic receptors are Lectins (recognize carbohydrates) or Scavenger receptor (recognize negatively charged ligands). There is a Mannose receptor, a Glucan receptor, and a LPS receptor |
|
|
Term
| signaling receptor function of the macrophage |
|
Definition
| Toll like receptor activation results in triggering of the cascade of the signaling pathway leading to the release of the transcriptional factor NF(kappa)B which induces expression & transcription of the inflammatory and immune responses genes, detects microbial components |
|
|
Term
| complement receptor function of the macrophage |
|
Definition
|
|
Term
|
Definition
Part of Innate immunity 1) C3 is cleaved in plasma into C3a and C3b 2) C3b attaches to pathogen surface 3) factor B binds C3b 4) factor D binds to C3b, and causes factor B to be cleaved into Bb and Ba 5)Bb attaches to C3b and factor D leaves 6) C3bBb is alternative C3 convertase 7) C3 convertase cleaves C3 into C3b and C3a 8) C3b can attach to pathogen surface OR attach to C3 convertase to create C5 convertase 9) C5 convertase cleaves C5 into C5b and C5a 10) C5b initiates membrane attack complex |
|
|
Term
|
Definition
Part of Innate Immunity 1) MBL binds to carbohydrates on the pathogen surface 2) MASPs becomes active via binding 3) MASPs cleave C4 into C4a and C4b, C4b attaches to pathogen surface 3a) MASPs cleave C2 into C2a and C2b, C2b attaches to C4b on surface 4) C4bC2b complex = classical/lectin C3 convertase 5) C3 convertase cleaves C3 into C3b and C3a, C3b binds to cell surface or binds to C3 convertase to turn it into C5 convertase 6) C5 convertase cleaves C5 into C5a and C5b, C5b initiates membrane attack complex |
|
|
Term
|
Definition
Part of adaptive and innate immunity 1) C reactive proteins or Ab bind to pathogen surface 2) C1 bind to C reactive proteins or Ab, C1 becomes active protease 3) C1s cleaves C4 into C4a (anaphylaxis) and C4b and C2 into C2a and C2b 4) C4b binds to pathogen surface, C2a binds to C4b (C4bC2a convertase aka C3 convertase) 5) C3 convertase can cleave C3 molecules into C3a and C3b, C3b attaches to C3 convertase to create the C3/C5 convertase 6) C3/C5 convertase cleaves C3 into C3a and C3b, C3b attaches to cell surface to induce phagocytosis 6a) C3/C5 convertase cleaves C5 into C5a and C5b, C5b initiates membrane attack complex |
|
|
Term
|
Definition
produced in the alternative pathway from factor D causing the cleavage of factor B into Bb and Ba. Bb associates with C3b on pathogen surface
C3 convertase cleaves C3 into C3b and C3a. C3b attaches to pathogen surface or associated with C3 convertase to create C5 convertase |
|
|
Term
|
Definition
produced in the classical pathway from C1s cleaving C4 and C2 and C4b and C2a binding to pathogen surface
produced in the lectin pathway from MASP protease cleaving both C4 and C2, and C4b and C2b associating and binding to cell surface
C3 convertase aka C4bC2a protease cleaves C3 into C3a and C3b. C3b binds to C3 convertase and creates C3/C5 convertase. |
|
|
Term
|
Definition
| initiates membrane attack complex |
|
|
Term
| Function of alternative convertases |
|
Definition
| C3bBb: continues cleavage of the soluble C3 molecules while bound to the pathogen surface |
|
|
Term
| Function of classical convertases |
|
Definition
| C4bC2a: component of both the lectin & classical pathways of complement activation. It binds & cleaves C3 to yield C3b fragment attached to the pathogen surface |
|
|
Term
|
Definition
| fragment acts as a chemoattractant which recruits phagocytes from blood circulation |
|
|
Term
|
Definition
| fragments are termed anaphylatoxins because sometime these inflammatory reactions can generalize & cause anaphylactic shock |
|
|