Exam 2 Innate Immunity Flashcards
First line of defense
- Skin with high pH, stratified epithelium, and microbiota
- next is mucous membrane which has columnar epithelium, cilia
- last is chemical barrier of defensins, acidic stomach, lactoferrin, and lysozyme
defensins
cationic antimicrobial peptides; destroy membrane of bacteria
lactoferrins
lock up iron
lysozyme
in tears/saliva and digests glycosidic bonds between NAM and NAG
progenitor cell of innate
lymphoid
progenitor cell of adaptive
myeloid –> macrophage progenitor
Phagocytes
Neutrophils (fast and short-lived-PMNs), Macrophages (long-lived), Eosinophils (motile-attack multicellular parasites)
Inflammatory cells
Mast Cells (histamine); non motile in serosa, capable of phagocytosis and involved in allergies (IgE)
Innate cells
Dendritic cells (initiate adaptive-phagocytic), NK cells (attack infected host and cancer cells-intra; can also kill extracellular with antibody)
Dendritic Cell
a phagocytic innate cell that will activate T cells b/c it is an APC
NK cells
innate killer cell; kills intracellular infected cells and also extracellular ones marked by antibodies
PAMPS
Pathogen Associated Molecular Patterns: highly conserved, not on humans, non-specific recognition using specific molecules such as LPS, peptidoglycans, flagella, and some ncltds
Binds PAMPs
PRR (pattern recognition receptor) and Toll-like receptor; also Macrophages and some innate cells; can be bound by antibodies and opsonized
binds opsonin
Fc receptors-recognize IgG
Opsonize PAMPS
C3b and IgG antibody
Phagocytes bind what on PAMPs
bind to opsonin (C3b) and engulfs/phagocytosis
Acute Inflammation
initial inflammation response to contain, destroy, and remove pathogens; move immune cells and inflammatory proteins to site; 5 R’s
5 R’s of Acute inflammation
Recognize (dead or foreign cells as PAMPS), Release (cytokines and chemokines released by Macrophages and histamine from Mast cells –> permeability), Recruit (WBC-lymphocytes via TNF-alpha and then diapedesis), Removal, Resolution
Fc Receptors
Recognize IgG antibody which recognizes antigens
Recruitment of WBC
- TNF-alpha upregulates adhesion proteins on surface of endothelial cells and WBC
- selectins bind musin on the WBC
- chemokines induce a change in integrins
- integrins firmly adhere to ICAMs stopping the WBC
Slows WBC
selectins and musin (on WBC)
Stops WBC
integrin (activated by chemokine) which binds to ICAM
upregulates adhesion proteins on epithelial cells and WBC
TNF-alpha
promotes crossing from vessel to tissue of WBC
chemotaxis-driven by chemokines (released by other WBC)
Left Shift
increase in band cells (PMNs) which means increased neutrophils which means a bacterial infection
increased total WBC
allergy or reaction
increased lymphocytes
viral infection
increased eosinophils
parasitic infection
chronic inflammation
buys time for adaptive response;
to contain, destroy, and remove persistent pathogens
first to arrive and first to die
neutrophils
Phagocytosis Steps
- Attaches (TLR/PRR to PAMP)
- engulfs –> forms phagosome
- fusion of phagosome and lysosome –> phagolysome
- killing and degradation
- non oxidative killing (not activated): lysosomes & peptides + lactoferrin
- oxidative killing (when activated): increase O2 to increase ROS - Exocytosis
Non oxidative killing
Killing of PAMP by means of phagolysosome by using lysosome, antimicrobial peptides that damage the membrane, or lactoferrin which binds iron
oxidative killing
Phagolysosome-when activated by M1 Macrophages only- will increase Oxygen use and produce ROS such as Nitric oxide which is toxic to cells
Proinflammatory cytokines include
- IL (mainly IL-1, and 6)
- Chemokines
- Tumor Necrosis Factor Alpha (TNF-alpha)
- Others
- -histamine
- -prostaglandins and interleukons
- -complement proteins (C3a and C5a)
Interleukens
mainly IL 1 and 6 for inflammation;
stimulate chemotaxis of PMNs!
Also: stimulates selection and prod. of epithelial cells and fever
Chemokines
direct WBC to location (chemotaxis)
TNF-alpha
stim production of adhesion proteins selectins on epithelial cells
Also: fever, vascular permeability, and NK cells